Cited by 248Cancer, Hypoxia, and MetabolismCancer, Lipids, and MetabolismMetabolism, Diabetes, and Cancer

The DOI matches its Crossref record; 135 of the 135 references it cites were found in a registry or an index.

Metabolic reprogramming in triple-negative breast cancer

Open access

Wang, Zhanyu, Jiang, Qianjin, Dong, Chenfang·2020·Cancer Biology and Medicine

DOI 10.20892/j.issn.2095-3941.2019.0210PMC PMC7142847

Open this paper in CoChat — free account

Abstract

Since triple-negative breast cancer (TNBC) was first defined over a decade ago, increasing studies have focused on its genetic and molecular characteristics. Patients diagnosed with TNBC, compared to those diagnosed with other breast cancer subtypes, have relatively poor outcomes due to high tumor aggressiveness and lack of targeted treatment. Metabolic reprogramming, an emerging hallmark of cancer, is hijacked by TNBC to fulfill bioenergetic and biosynthetic demands; maintain the redox balance; and further promote oncogenic signaling, cell proliferation, and metastasis. Understanding the mechanisms of metabolic remodeling may guide the design of metabolic strategies for the effective intervention of TNBC. Here, we review the metabolic reprogramming of glycolysis, oxidative phosphorylation, amino acid metabolism, lipid metabolism, and other branched pathways in TNBC and explore opportunities for new biomarkers, imaging modalities, and metabolically targeted therapies.

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

Integrity signals

Registry

Crossref · 10.20892/j.issn.2095-3941.2019.0210

Cites

135 of 135 references verified0 citation errors · 0 not checkable

Statistics

Figure 1 Metabolic reprogramming in triple-negative breast cancer (TNBC). TNBC upregulates several key glycolytic enzymes and transporters such as GLUT, HK, LDH, and MCT, therefore displaying high rate of glycolysis and glycolytic branched pathways, including serine synthesis and pentose phosphate pathway (PPP) for NADPH generation, and hexosamine biosynthetic pathway (HBP) for protein glycosylation. Other pathways such as fatty acid oxidation (FAO), glutaminolysis and cystine uptake are also induced in TNBC to meet its bioenergetic or biosynthetic demands, and mitigate reactive oxygen species (ROS) that is generated from oxidative phosphorylation (OXPHOS). Enzymes that are upregulated in TNBC are shown as light-yellow ovals, and enzymes downregulated in TNBC are shown as gray ovals.CC BY · PubMed Central

Figure 2 Switchable metabolic dependence on glycolysis and oxidative phosphorylation (OXPHOS) regulated by HIF-1α and AMPK. Under normoxic condition, HIF-1α is hydroxylated and subsequently degraded by PHD2 in an α-KG- and cysteine-dependent manner. In TNBC, decreased levels of α-KG and cysteine due to altered activity of transketolase (TKT) and xCT cystine/glutamate antiporter, respectively, contribute to normoxic activation of HIF-1α signaling, which triggers aerobic glycolysis with the upregulation of glycolysis-related enzymes and transporters. Although TNBC cells rely on glycolysis for rapid proliferation, OXPHOS which generate ATP more efficiently is also required, especially under bioenergetic stress. Activated AMPK and Myc pathways induce mitochondrial biogenesis and enzymes involved in glutaminolysis and fatty acid oxidation (FAO) to facilitate OXPHOS, thus endowing TNBC with metabolic plasticity to switch between glycolysis and OXPHOS. In addition, AMPK signaling also promotes epithelial-mesenchymal transition (EMT) through regulating lipid metabolism and increases the secretion of cytokines to recruit immunosuppressive myeloid-derived suppressor cells (MDSCs). Many drugs have been developed to target these key processes in the metabolic reprogramming of TNBC.CC BY · PubMed Central

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

1 retracted

RETRACTED: PHGDH Expression Is Required for Mitochondrial Redox Homeostasis, Breast Cancer Stem Cell Maintenance, and Lung Metastasis
Samanta, D., Park, Y., Andrabi, S. A., Shelton, L. M., Gilkes, D. M., & Semenza, G. L. (2016) · Cancer Research · doi:10.1158/0008-5472.can-16-0530 · Cited by 242 · cited 1×
“This metabolic reprogramming maintains the level of NADPH to counter hypoxia-or chemotherapy-induced ROS stress and plays a role in BCSC enrichment and lung metastasis 53,54 .”
Background
Retracted
Evaluation of Factors Related to Late Recurrence - Later than 10 Years after the Initial Treatment - in Primary Breast Cancer
Nishimura, R., Osako, T., Nishiyama, Y., Tashima, R., Nakano, M., Fujisue, M., Toyozumi, Y., & Arima, N. (2013) · Oncology · doi:10.1159/000353099 · Cited by 13,239
The emerging hallmarks of cancer metabolism
Pavlova, N. N., & Thompson, C. B. (2016) · Cell Metabolism · doi:10.1016/j.cmet.2015.12.006 · Cited by 5,926 · cited 1×
“…despite the availability of adequate oxygen (known as aerobic glycolysis or the Warburg effect), thereby maintaining high levels of glycolytic intermediates for biosynthetic requirements, while decreasing the production of reactive oxygen species (ROS) from oxidative phosphorylation (OXPHOS) 6 .”
Background
Regulation of cancer cell metabolism
Cairns, R. A., Harris, I. S., & Mak, T. W. (2011) · Nature Reviews Cancer · doi:10.1038/nrc2981 · Cited by 4,744 · cited 2×
“Under normoxic conditions, HIF-1 α is hydroxylated by the proline hydroxylase domain (PHD2; also known as EglN1) in an oxygen-and α -ketoglutarate ( α -KG)- dependent manner, which results in its ubiquitination and subsequent degradation 15 .”
Background
Triple-Negative Breast Cancer
Foulkes, W. D., Smith, I. E., & Reis-Filho, J. S. (2010) · New England Journal of Medicine · doi:10.1056/nejmra1001389 · Cited by 4,719
Strategies for subtypes—dealing with the diversity of breast cancer: highlights of the St Gallen International Expert Consensus on the Primary Therapy of Early Breast Cancer 2011
Goldhirsch, A., Wood, W. C., Coates, A. S., Gelber, R. D., Thurlimann, B. J. K., & Senn, H.-J. (2011) · Annals of Oncology · doi:10.1093/annonc/mdr304 · Cited by 3,836
Metabolic Reprogramming: A Cancer Hallmark Even Warburg Did Not Anticipate
Ward, P. S., & Thompson, C. B. (2012) · Cancer Cell · doi:10.1016/j.ccr.2012.02.014 · Cited by 3,233 · cited 1×
“This rewired metabolic network depends on the dysregulation of many key enzymes, such as pyruvate kinase muscle isozyme M2 (PKM2), which redirects glycolytic intermediates into the anabolic pathway 7 .”
Background
Response to neoadjuvant therapy and long-term survival in patients with triple-negative breast cancer
Liedtke, C., Mazouni, C., Hess, K. R., André, F., Tordai, A., Mejia, J. A., Symmans, W. F., Gonzalez-Angulo, A. M., Hennessy, B., Green, M., et al. (2008) · Journal of Clinical Oncology · doi:10.1200/jco.2007.14.4147 · Cited by 2,892 · cited 1×
“Nevertheless, chemotherapy currently remains the mainstay of systemic treatment due to the lack of effective targeted therapy such as anti-HER2 and anti-ER 5 .”
Background
EMT, CSCs, and drug resistance: the mechanistic link and clinical implications
Shibue, T., & Weinberg, R. A. (2017) · Nature Reviews Clinical Oncology · doi:10.1038/nrclinonc.2017.44 · Cited by 2,539 · cited 1×
“EMT confers TNBC with cancer stem cell (CSC)-like characteristics, including elevated metastatic potential and enhanced resistance to chemotherapy 4 .”
Background
From Krebs to clinic: glutamine metabolism to cancer therapy
Altman, B. J., Stine, Z. E., & Dang, C. V. (2016) · Nature Reviews Cancer · doi:10.1038/nrc.2016.71 · Cited by 2,119

Show all 135 references

Sorted by citations

Items 101–200 of 248

Serum and Fecal Metabolite Profiles Linking With Gut Microbiome in Triple-Negative Breast Cancer Patients
Liu, J., Shi, J., Zhang, T., Chen, M., Li, Z., Lu, C., & Wang, F. (2024) · Breast Cancer Basic and Clinical Research · doi:10.1177/11782234241285645 · Cited by 7
Ketogenesis promotes triple-negative breast cancer metastasis via calpastatin β-hydroxybutyrylation
Jiang, H., Zeng, Y., Yuan, X., Chen, L., Xu, X., Jiang, X., Li, Q., Li, G., & Han, Y. (2024) · Lipids in Health and Disease · doi:10.1186/s12944-024-02364-x · Cited by 7
Mapping molecular landscapes in triple-negative breast cancer: insights from spatial transcriptomics
Al-Mansour, F. S. H., Almasoudi, H. H., & Albarrati, A. (2025) · Naunyn-Schmiedeberg s Archives of Pharmacology · doi:10.1007/s00210-025-04057-3 · Cited by 7
“Similarly, chemotherapy-resistant TNBC regions identified through ST exhibit adaptive metabolic rewiring, where oxidative phosphorylation (OXPHOS)- dependent tumor cells compensate for glycolysis inhibition by upregulating mitochondrial biogenesis pathways (Wang et al. 2020).”
Inhibiting glycolysis facilitated checkpoint blockade therapy for triple-negative breast cancer
Li, C., Tang, Y., Zhang, R., Shi, L., Chen, J., Zhang, P., Zhang, N., & Li, W. (2025) · Discover Oncology · doi:10.1007/s12672-025-02320-w · Cited by 7
“HK2-mediated metabolic reprogramming in TNBC also affects the tumor microenvironment (TME) [10].”
Sialylated IgG expressed in triple-negative breast cancer cells promotes cancer progression by promoting glycolysis
Hu, C., Zhang, S., Duan, F., Huang, X., Huang, J., Zhu, Z., Mo, X., Xu, W., Wu, L., Fan, Z., et al. (2025) · Breast Cancer Research · doi:10.1186/s13058-025-02052-3 · Cited by 7
“They display elevated glucose uptake and lactate secretion, with the upregulation of several key glycolytic enzymes and transporters, including hexokinase (HK), lactate dehydrogenase (LDH), and monocarbox-ylate transporter (MCT) etc. [37, 38].”
Hsa_circ_0052611 and mir-767-5p guide the warburg effect, migration, and invasion of BRCA cells through modulating SCAI
Wang, X., Liu, Z., Chu, A., Song, R., Liu, S., Chai, T., & Sun, C. (2023) · Journal of Bioenergetics and Biomembranes · doi:10.1007/s10863-023-09985-4 · Cited by 7
“and Martel 2018; Wang et al. 2020).”
Alteration of DNA Methyltransferases by Eribulin Elicits Broad DNA Methylation Changes with Potential Therapeutic Implications for Triple-Negative Breast Cancer
Bagheri, M., Lee, M. K., Muller, K. E., Miller, T. W., Pattabiraman, D. R., & Christensen, B. C. (2024) · Epigenomics · doi:10.2217/epi-2023-0339 · Cited by 7
TRIM34 inhibits triple-negative breast cancer progression by attenuating fatty acid synthesis via facilitating FASN ubiquitination
Li, Y., Shan, J., Liu, S., Shen, Y., Niu, L., Mao, Q., & Chen, X. (2025) · Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease · doi:10.1016/j.bbadis.2025.167958 · Cited by 8
The lactylation index predicts the immune microenvironment and prognosis of pan-cancer patients
ZHAI, X., LIU, J., Xiao, J.-W., Zhang, T., Wang, J., LI, J., & YU, S. (2024) · Biocell · doi:10.32604/biocell.2024.050803 · Cited by 6
Systematic profiling of mitochondria-related transcriptome in tumorigenesis, prognosis, and tumor immune microenvironment of intrahepatic cholangiocarcinoma: a multi-center cohort study
Chen, B., Lü, M., Chen, Q., Zou, E., Bo, Z., Li, J., Zhao, R., Zhao, J., Yu, Z., Chen, G., et al. (2024) · Frontiers in Genetics · doi:10.3389/fgene.2024.1430885 · Cited by 6
Application of Metabolic Biomarkers in Breast Cancer: A Literature Review
Lee, A., & Lam, C. (2025) · Annals of Laboratory Medicine · doi:10.3343/alm.2024.0482 · Cited by 7
Metabolomics as a tool for understanding and treating triple-negative breast cancer
Khan, G., Hussain, M. S., Ahmad, S., Alam, N., Ali, S., & Alam, P. (2025) · Naunyn-Schmiedeberg s Archives of Pharmacology · doi:10.1007/s00210-025-04234-4 · Cited by 6
“Furthermore, TNBC cells demonstrate altered AA metabolism, particularly an increased reliance on glutamine metabolism (Wang et al. 2020).”
Peptide Hydrogels for Renal Carcinoma Therapy via Synergistic Inhibition of Glycolysis and Mitochondrial Metabolism Reprogramming
Ge, Z., Xu, J., Meng, F., Sun, M., He, L., Fan, Z., & Du, J. (2025) · ACS Applied Materials & Interfaces · doi:10.1021/acsami.5c06429 · Cited by 6
Triple negative breast cancer migration is modified by mitochondrial metabolism alteration induced by natural extracts of C. spinosa and P. alliacea
Carlosama, C., Arévalo, C., Jiménez, M. C., Lasso, P., Urueña, C., Fiorentino, S., & Barreto, A. (2024) · Scientific Reports · doi:10.1038/s41598-024-70550-z · Cited by 4
Identification of a Gene Expression Signature to Predict the Risk of Early Recurrence and the Degree of Immune Cell Infiltration in Triple-negative Breast Cancer
Sato, K., MIURA, K., Tamori, S., & Akimoto, K. (2024) · Cancer Genomics & Proteomics · doi:10.21873/cgp.20450 · Cited by 9
PLA2G4F is a metabolic checkpoint in triple-negative breast cancer: Insights from multiple omics analysis and experiments
Tang, X., Jiang, N., Kou, Y., Cheng, S., & Yan, F. (2025) · Molecular Therapy Oncology · doi:10.1016/j.omton.2025.200963 · Cited by 5
Integrating of serum pharmacochemistry, metabolomics, and experimental validation to explore the mechanism of Erzhi Pill against Triple-negative breast cancer
Qi, Y., Li, P., Li, B., Lv, P., Hu, H. H., Tan, C., Wang, W., Jiang, Y., & He, J. (2025) · Journal of Ethnopharmacology · doi:10.1016/j.jep.2025.120287 · Cited by 5
Lactate and lactylation in breast cancer: current understanding and therapeutic opportunities
Huang, L. J., Chen, X., Yan, M., Xiang, Z., & Wu, J. (2025) · Cancer Biology and Medicine · doi:10.20892/j.issn.2095-3941.2025.0173 · Cited by 6
A Natural LDHA Allosteric Inhibitor Geraniin Suppresses Triple‐Negative Breast Cancer Cell Growth
Yu, Y. P., Ye, X., Hou, T., Zhou, H., Liu, L., Yuan, W., Wang, J., & Liang, X. (2025) · Phytotherapy Research · doi:10.1002/ptr.70112 · Cited by 5
Bioactive Natural Compounds in Triple-Negative Breast Cancer: Molecular Targets and Therapeutic Perspectives
Jiménez-Flores, E., Reytor-González, C., Gavilanes, D. J., Carrillo, C., Horowitz, R., Carrera, J. C. C., Ordóñez, G. D. B., & Simancas‐Racines, D. (2026) · Pharmaceuticals · doi:10.3390/ph19040550 · Cited by 6
Prediction of prognosis and immunotherapy efficacy based on metabolic landscape in lung adenocarcinoma by bulk, single-cell RNA sequencing and Mendelian randomization analyses
Liu, Y., Zhang, X., Pang, Z., Wang, Y., Zheng, H., Wang, G., Wang, K., & Du, J. (2024) · Aging · doi:10.18632/aging.205838 · Cited by 5
The signature of extracellular vesicles in hypoxic breast cancer and their therapeutic engineering
Zhu, B., Xiang, K., Li, T., Li, X., & Shi, F. (2024) · Cell Communication and Signaling · doi:10.1186/s12964-024-01870-w · Cited by 5
“The robust antioxidation sys-tem of TNBC can rapidly synthesize a large amount of GSH to counteract the transient increase in ROS and the enzymes involved, including malic enzyme 1 and nicotinamide phosphoribosyltransferase, which do not depend on HER2 [136].”
Background
FAK and p130Cas Modulate Stiffness‐Mediated Early Transcription and Cellular Metabolism
Tumenbayar, B., Pham, K., Biber, J. C., Tutino, V. M., Brazzo, J. A., Yao, P., & Bae, Y. (2024) · Cytoskeleton · doi:10.1002/cm.21971 · Cited by 5
“…(Alzheimer's, Parkinson's, and Huntington diseases), all involving altered metabolism and biosynthesis (Chong, Clarke, and Levelt 2017; Encarnacion-Rosado and Kimmelman 2021; Kang, Lee, and Lee 2017; Nambron et al. 2016; Sonninen et al. 2020; Vanhove et al. 2019; Wang, Jiang, and Dong 2020).”
UPLC-MS/MS-based Lipidomic Profiles Revealed Aberrant Lipids Associated with Invasiveness of Silent Corticotroph Adenoma
Wang, Z., Guo, X., Wang, W., Gao, L., Bao, X., Feng, M., Lian, W., Zhu, H., & Xing, B. (2020) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/clinem/dgaa708 · Cited by 5
SOX4-SMARCA4 complex promotes glycolysis-dependent TNBC cell growth through transcriptional regulation of Hexokinase 2Preprint
Khanna, P., Mehta, R. N., Mehta, G. A., Bhatt, V. D., Guo, J. Y., & Gatza, M. L. (2023) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2023.09.10.557071 · Cited by 5
Polydopamine‐Integrated Nanomedicine through Dual Metabolic Intervention with Enhanced Photothermal Therapy against Triple‐Negative Breast Cancer
Xu, C., Gao, Y., Zhang, X., Jia, F., Pan, Z., Li, M., Wang, W., Li, X., & Wu, Y. F. (2025) · Advanced Therapeutics · doi:10.1002/adtp.202400570 · Cited by 4
Reopening Pandora’s box: Is there a role for HDL in breast cancer?
Sawada, M. I., Santana, M. B. S., Vancini, M. G., & Passarelli, M. (2025) · Seminars in Cancer Biology · doi:10.1016/j.semcancer.2025.07.001 · Cited by 4
Dissecting the Non-Immune Tumor Microenvironment in Triple-Negative Breast Cancer: Molecular Subtype-Specific Patterns and Prognostic Implications
Syrnioti, A., Timotheadou, E. T., Papadopoulos, V. N., Syrnioti, G., & Κoletsa, T. (2025) · International Journal of Molecular Sciences · doi:10.3390/ijms262211211 · Cited by 4
“…fibroblasts (CAFs), vascular structures, adipose tissue, extracellular matrix (ECM) components, and metabolic gradients play critical roles in creating a complex and dynamic ecosystem, with a direct impact on tumor growth, invasion, therapeutic resistance, and metastatic potential [17–20].”
Overcoming Therapeutic Resistance in Triple-Negative Breast Cancer: Targeting the Undrugged Kinome
Lee, C. H., Nguyen, T. M., Lee, Y., Choi, S. G., Nguyễn, P. N., Park, J. H., & Park, M. K. (2025) · International Journal of Molecular Sciences · doi:10.3390/ijms27010450 · Cited by 8
Electrochemical platform for in situ metabolic profiling and therapeutic evaluation of triple-negative breast cancer
Koo, K., Kim, C.-D., Kim, H., Wi, J.-K., Kim, H., Shin, Y.-Z., Cha, H., Kang, S. H., & Kim, T.-H. (2026) · Chemical Engineering Journal · doi:10.1016/j.cej.2026.173253 · Cited by 4
Bibliometric analysis of phosphoglycerate kinase 1 expression in breast cancer and its distinct upregulation in triple-negative breast cancer
Chen, J., Li, J., He, R., Huang, Z., Chen, G., & Zou, W. (2024) · World Journal of Clinical Oncology · doi:10.5306/wjco.v15.i7.867 · Cited by 4
LC-MS Orbitrap-based metabolomics using a novel hybrid zwitterionic hydrophilic interaction liquid chromatography and rigorous metabolite identification reveals doxorubicin-induced metabolic perturbations in breast cancer cells
Abdelrazig, S., McCabe, Á., Yasin, A., Chaudhary, R., Ochsenkühn, M. A., Scicchitano, D. A., & Amin, S. A. (2025) · RSC Advances · doi:10.1039/d5ra01044f · Cited by 4
Isoform switching leads to downregulation of cytokine producing genes in estrogen receptor positive breast cancer
Khan, M. S., Hanif, W., Alsakhen, N. A., Jabbar, B., Shamkh, I. M., Alsaiari, A. A., Almehmadi, M. M., Alghamdi, S. A., Shakoori, A. M., Farraj, D. A. A., et al. (2023) · Frontiers in Genetics · doi:10.3389/fgene.2023.1230998 · Cited by 4
“However, ER + tumors are glutamine-independent and show increased GLUD expression (Wang et al., 2020).”
Background
Phytosesquiterpene lactones deregulate mitochondrial activity and phenotypes associated with triple-negative breast cancer metastasis
Cheng, Y., Chang, D.-M., Tung, Y., Hsiao, P., Nakagawa‐Goto, K., & Shyur, L. (2024) · Phytomedicine · doi:10.1016/j.phymed.2024.156226 · Cited by 4
The diverse metabolic heterogeneity of stem cells in a BRCA+/-breast cancer population
Gramatiuk, S. M., Bagmut, I. Y., Sheremet, M. I., Maksymyuk, V. V., Tarabanchuk, V. V., & Moroz, P. V. (2021) · Journal of Medicine and Life · doi:10.25122/jml-2020-0105 · Cited by 4
Diet and Cancer Metabolic Reprogramming
Bhattacharya, S. (2021) · Cancer Reports and Reviews · doi:10.15761/crr.1000233 · Cited by 4
Identification of ubiquitination-related gene classification and a novel ubiquitination-related gene signature for patients with triple-negative breast cancer
Zhao, K., Zheng, Y., Lu, W., & Chen, B. (2023) · Frontiers in Genetics · doi:10.3389/fgene.2022.932027 · Cited by 4
Efficient metabolic fingerprinting profiling of extracellular vesicles for precise cancer diagnosis and treatment monitoring
Wang, S., Liu, D., Wang, R., Zou, Y., Tian, T., Huang, X., Fang, X., & Liu, B. (2025) · Materials Today Bio · doi:10.1016/j.mtbio.2025.101857 · Cited by 3
“Some studies reported that the protein related to the serine metabolic pathway was highly expressed in triple-negative breast cancer (TNBC) [41], which was consistent with up-regulation of serine in esBC-EVs.”
Baicalin‐Loaded Bifunctional Albumin Nanoparticles Inhibit Triple‐Negative Breast Cancer Growth by Remodeling the Inflammatory Microenvironment
Liu, F., Meng, F., Hong, X., Giri, A. K., Asim, M. H., Chen, Z., Chen, Y., Lin, Y., He, L., Bu, Q., et al. (2025) · Advanced Healthcare Materials · doi:10.1002/adhm.202502251 · Cited by 5
Fucosylated N-Glycan Landscape of Triple-Negative Breast Cancer
Scott, D. A., Seal, S., Spruill, L., Dunne, J., Colditz, G. A., Mehta, A. S., Drake, R. R., Ford, M. E., & Angel, P. M. (2025) · Molecular Cancer Research · doi:10.1158/1541-7786.mcr-25-0483 · Cited by 3
Exogenous kisspeptin-10 treatment shows pleiotropy via induction of KISS1 expression, metastasis suppression, and promotes apoptosis in triple-negative breast cancer
Shah, H., Mohan, A. M., Buch, L., Ramachandran, A. V., & Pandya, P. (2025) · Scientific Reports · doi:10.1038/s41598-025-19140-1 · Cited by 4
Identification and analysis of metabolic reprogramming-related genes in triple-negative breast cancer
Kong, H., Pan, M., & Sun, L. (2025) · Clinical and Experimental Medicine · doi:10.1007/s10238-025-01870-1 · Cited by 4
“…the tumor to meet its bioenergetic and biosynthetic needs, maintain redox balance, and fuel oncogenic signaling, proliferation, and metastasis [24] Advances in computational technologies, including machine learning and network pharmacology, have revolutionized the identification of illness…”
Lipocalin-2 in Triple-Negative Breast Cancer: A Review of Its Pathophysiological Role in the Metastatic Cascade
Keller, D. T., Weiskirchen, R., & Schröder, S. K. (2025) · International Journal of Molecular Sciences · doi:10.3390/ijms262210938 · Cited by 4
“Conversely, TNBC shows upregulation of genes related to glucose uptake and lactate metabolism [77].”
Apocrine carcinoma of the breast: distinctive metabolic reprogramming and high‐frequency PIK3CA mutations revealed by molecular and immunohistochemical analysis
Nakamura, H., Kukita, Y., Kittaka, N., Kusama, H., Nakayama, T., Tamaki, Y., Yoshida, K., Kunimasa, K., Imamura, F., & Yagi, T. (2025) · Histopathology · doi:10.1111/his.70024 · Cited by 3
Emerging small molecule strategies target cancer stem cells through ferroptosis and metabostemness
Farah, H. S., Abdulsahib, W. K., Ismail, S. H., Roopashree, R., Ray, S., Nandhini, S. U., Arora, V., Chauhan, A. S., & Buriyeva, D. (2025) · Discover Oncology · doi:10.1007/s12672-025-04259-4 · Cited by 5
“Similarly, Sulfasalazine, a drug for inflammatory conditions, has demonstrated anti-cancer effects by inhibiting xCT (System Xc-) activity, thereby retarding the growth of triple-negative breast cancer (TNBC) in vitro by inducing ferroptosis [77].”
Influential
Anticancer Effect of Pacificusoside D from the Starfish Solaster pacificus in Combination with 2-Deoxy-D-glucose on Oxidative Phosphorylation in Triple-Negative Breast Cancer Cells MDA-MB-231
Malyarenko, O. S., Malyarenko, T. V., Kicha, A. A., Ermakova, S. P., & Ivanchina, N. V. (2026) · Marine Drugs · doi:10.3390/md24020075 · Cited by 3
Metabolic Vulnerabilities as a Therapeutic Target in Breast Cancer
Guo, S., & Addison, C. (2026) · Current Oncology · doi:10.3390/curroncol33020129 · Cited by 4
“Aerobic glycolysis use is a common metabolic feature across breast cancer subtypes, with TNBC being the most reliant on this process [33–35], and breast cancers show significant upregulation of numerous glycolytic enzymes.”
A Lamp2a-linked RNA secreted by ADSCs prevents ENO1–lactylation–glycolysis feedback and cell malignant behavior in triple-negative breast cancer
Cheng, S., Xia, B., Li, L., Zhao, S., Zhang, Q., Hui, X., Liu, X., Xiong, W., Chen, W., & Zhang, Y. (2026) · Cell Death and Disease · doi:10.1038/s41419-026-08517-3 · Cited by 3
“In TNBC samples, we found that ENO1 mRNA levels are lowest in the MSL subtype and highest in the BL subtype of TNBC. Interestingly, compared with other breast cancer subtypes, TNBC is more reliant on glycolysis, exhibiting increased glucose uptake and lactate secretion [41].”
Discovery of aminothiazole derivatives as a chemical scaffold for glutaminase inhibition
Costa, R. K. E., Brancaglion, G. A., Pinheiro, M. P., Adamóski, D., da Silva, B. N., Negrão, C. V. Z. D. V., Gonçalves, K. D. A., Rodrigues, C. T., Ambrosio, A. L. B., Guido, R. V. C., et al. (2023) · Results in Chemistry · doi:10.1016/j.rechem.2023.100842 · Cited by 3
Integrated stress response-upregulated mitochondrial SLC1A5var enhances glucose dependency in human breast cancer cells in vitro
Wang, S., Ho, Y.-C., Chou, C., Chang, Y., Lee, H., & Tseng, L. (2024) · The International Journal of Biochemistry & Cell Biology · doi:10.1016/j.biocel.2024.106688 · Cited by 3
Pan-cancer molecular signatures connecting aspartate transaminase to cancer prognosis, metabolic and immune signatures
Siwo, G., Singal, A. G., & Waljee, A. K. (2026) · Frontiers in Oncology · doi:10.3389/fonc.2026.1727389 · Cited by 3
Molecular and therapeutic bases of cancer
Fajardo-Orduña, G. R., & Chamorro-Plata, D. (2021) · Elsevier eBooks · doi:10.1016/b978-0-12-819828-5.00002-4 · Cited by 3
High Expression of RAI14 in Triple-Negative Breast Cancer Participates in Immune Recruitment and Implies Poor Prognosis Through Bioinformatics Analyses
Cui, R., Zhao, T., Bai, C., Ji, N., Hua, J., Ren, L., & Li, Y. (2022) · Frontiers in Pharmacology · doi:10.3389/fphar.2022.809454 · Cited by 3
Tumor-infiltrating lymphocytes display prognostic signatures associated with chemotherapy response in TNBC patients
Banerjee, S., Tiwari, V. K., Raman, K., & Inayatullah, M. (2026) · iScience · doi:10.1016/j.isci.2026.116295 · Cited by 2
Dual inhibitor of MDM2 and NFAT1 for experimental therapy of breast cancer: in vitro and in vivo anticancer activities and newly discovered effects on cancer metabolic pathways
Wang, W., Aguilar, M., Datta, S., Alley, A., Tadesse, M., Wang, X., Gao, X., & Zhang, R. (2025) · Frontiers in Pharmacology · doi:10.3389/fphar.2025.1531667 · Cited by 3
Integrative Raman Spectroscopy and Multi-Omics Analysis of Lipid and Matrix Protein Heterogeneity in Triple-Negative Breast Cancer
Sheikh, E., Salim, K., Guttula, P. K., Burk, D. H., Belgodere, J. A., Beavers, W. N., Stephanes, N. M., Agrawal, K., Dubansky, B. H., Donnarumma, F., et al. (2025) · Chemical & Biomedical Imaging · doi:10.1021/cbmi.5c00104 · Cited by 2
The implied dysregulated RKIP-hypoxia axis in cancer and immune evasion: Clinical implications
McWhorter, R., Chouaı̈b, S., & Bonavida, B. (2025) · Drug Resistance Updates · doi:10.1016/j.drup.2025.101328 · Cited by 2
Spatial metabolomics atlas in the progression of oral squamous cell carcinoma
Zhao, H., Han, W., Shi, C., Luo, G., Lu, W., Fu, Y., Hu, Q., Song, X., Shang, Z., & Yang, X. (2025) · Journal of Translational Medicine · doi:10.1186/s12967-025-07421-2 · Cited by 2
“A defining characteristic of cancer cells is metabolic reprogramming, which alters metabolic pathways to satisfy the increased energy demands of proliferating cancer cells [6, 7].”
A Combined SIRT5 Activation and SIRT3 Inhibition Prevents Breast Cancer Spheroids Growth by Reducing HIF-1α and Mitophagy
Barreca, F., Aventaggiato, M., Cristina, M., Sansone, L., Belli, M., Lista, M. B., Francisci, G., Valente, S., Rotili, D., Mai, A., et al. (2025) · Pharmaceuticals · doi:10.3390/ph19010023 · Cited by 2
“In triple negative breast cancer cells, glutaminase (GLS) is overexpressed, and this is associated with high-grade metastatic breast cancer [5].”
Preclinical Study of CDH3-Targeted 89 Zr/ 177 Lu Theranostics in Triple-Negative Breast Cancer
Tang, M., Zhang, H., Du, H., Hao, X., Lin, B., Zhu, Y., Wang, D., Wu, W., & Du, X. (2026) · Molecular Pharmaceutics · doi:10.1021/acs.molpharmaceut.5c01584 · Cited by 2
LDHB Deficiency in Fibroblasts Induces Lactate-Mediated Inflammatory Reprogramming That Promotes Breast Cancer Metastasis
Luo, Z., Li, K., Yu, Y., Liu, Y., Weng, H., Zeng, X., Zheng, Y., & Li, W. (2026) · Cancer Research · doi:10.1158/0008-5472.can-25-2792 · Cited by 2
Multi-omics analyses related to mitochondria and ageing in triple-negative breast cancer implicate PYCR1 potentiates tumor progression
Huang, J., Hu, J., Shi, C., Chu, C., & Hu, H. (2026) · Cancer Cell International · doi:10.1186/s12935-026-04235-0 · Cited by 2
“Meanwhile, TNBC is distinct from other breast cancer subtypes due to its metabolic phenotype, which is predominantly characterized by mitochondrial metabolism [10].”
Mitochondrial biology and immune crosstalk in breast cancer: therapeutic opportunities and challenges
Zeng, Y., & Guo, Y. (2026) · Frontiers in Immunology · doi:10.3389/fimmu.2026.1715998 · Cited by 2
Suboptimal folic acid exposure rewires oncogenic metabolism and proteomics signatures to mediate human breast cancer malignancy
Huang, A., Huang, S.-Y., SHAH, P. M., Ku, W., Huang, K., Liu, Y., Su, C., & Huang, R.-F. S. (2022) · The Journal of Nutritional Biochemistry · doi:10.1016/j.jnutbio.2022.109000 · Cited by 3
Global transcriptome profiling of ST09 treated breast cancer cells identifies miR-197-5p/GPX3 antioxidant axis as a regulator of tumorigenesis
Nirgude, S., Desai, S. S., Ravindran, F., Mhatre, A., Mahadeva, R., Sharma, S., Rai, P. K., Shahana, M., V, Thumsi, J., & Choudhary, B. (2025) · International Immunopharmacology · doi:10.1016/j.intimp.2025.114127 · Cited by 2
Rewired glycolysis by DTL accelerates oncometabolite L-lactate generation to promote breast cancer progression
Liu, Y.-H., Li, J.-T., Cao, Y.-R., & Lv, M.-Z. (2025) · Frontiers in Oncology · doi:10.3389/fonc.2025.1583752 · Cited by 3
“Metabolic reprogramming, a well-established cancer hallmark, manifests in BC through enhanced glycolysis and anabolic ﬂ ux to sustain uncontrolled proliferation and survival (9, 10).”
Machine learning and single-cell analysis uncover distinctive characteristics of CD300LG within the TNBC immune microenvironment: experimental validation
Zhu, B., Wan, H., Ling, Z., Jiang, H., & Pei, J. (2025) · Clinical and Experimental Medicine · doi:10.1007/s10238-025-01690-3 · Cited by 2
“Consequently, an in-depth analysis of the molecular mechanisms underlying TNBC and the identification of effective therapeutic targets have emerged as key priorities and challenges in current research [7, 8].”
Targeting the METTL3/YTHDF3/m6A/PGK1 axis to combat Choriocarcinoma progression
Wang, D., Meng, C., Fan, J., Tang, S., & Fang, J. (2025) · Archives of Biochemistry and Biophysics · doi:10.1016/j.abb.2025.110550 · Cited by 2
Metabolic Reprogramming in Kidney Cancer: Implications for Therapy
Edo, E. T. (2025) · annals of urologic oncology · doi:10.32948/auo.2025.06.02 · Cited by 2
“Metabolic alterations also carry prognostic significance— elevated FDG-PET avidity correlates with aggressive tumor behavior [83], while high expression of glycolytic enzymes (HK2, LDHA) and glutamine transporters (ASCT2) predicts poor survival outcomes [84].”
Energy and endoplasmic reticulum stress induction by gold(III) dithiocarbamate and 2-deoxyglucose synergistically trigger cell death in breast cancer
Orobator, O. N., Mertens, R. T., Obisesan, O. A., & Awuah, S. G. (2024) · Journal of Biological Chemistry · doi:10.1016/j.jbc.2024.107949 · Cited by 1
Design, synthesis and biological evaluation of new SIRT3 activators for the treatment of triple-negative breast cancer
Huang, G., Wang, H., Zhao, X., Wang, C., Zhang, J. C., Yao, D., & Li, C. (2024) · Bioorganic & Medicinal Chemistry · doi:10.1016/j.bmc.2024.118040 · Cited by 1
Triple Negative Breast Cancer Heterogeneity and Tumour Microenvironment-based Model Systems’ Focus on Druggable Targets
Kundu, S., & Suresh, P. K. (2025) · Current Molecular Medicine · doi:10.2174/0115665240387430250508080548 · Cited by 2
REPROGRAMMING OF GLUCOSE METABOLISM IN HUMAN BREAST CANCER CELLS AFTER CO-CULTIVATION WITH BIFIDOBACTERIUM ANIMALIS
KOZAK, T., LYKHOVA, O., & Chekhun, V. F. (2025) · Experimental Oncology · doi:10.15407/exp-oncology.2025.01.003 · Cited by 1
“The most pronounced changes in metabolic activity toward increased glycolysis were observed in the luminal sub-type BC cells, probably because MDA-MB-231 cells of the basal subtype have already prefered this pathway of glucose metabolism [33].”
Integrated multi-omics analysis identifies SELENOP and PKMYT1 as immune-metabolic hub genes in breast cancer
Tang, G., Zhang, Z., Pang, B., Li, R., Liu, Y., Cai, H., Wang, W., Chen, C., Ou, Y., & Yang, Q. (2025) · Biochemistry and Biophysics Reports · doi:10.1016/j.bbrep.2025.102198 · Cited by 1
“…cells reprogram their metabolism in response to the nutrient-poor tumor microenvironment, utilizing metabolic reprogramming through glycolysis, oxidative phosphorylation, amino acid metabolism, lipid metabolism, and other metabolic pathways to meet bioenergetic and biosynthetic demands [6,7].”
Nutrient-transporter driven cytotoxic potential: an emerging nanotherapeutic approach
Dighe, S., Manchanda, N., Sharma, S., & Jain, S. (2025) · Drug Discovery Today · doi:10.1016/j.drudis.2025.104478 · Cited by 1
ATR-FTIR spectroscopic analysis of lipids and partial least squares analysis: the early detection of breast cancers
Walpita, P., Manage, S. A., Gunawardana, D. N., Gunasekara, B., Keerthi, A. A. P., Haputhanthri, P. R., & Perera, M. (2025) · Spectrochimica Acta Part A Molecular and Biomolecular Spectroscopy · doi:10.1016/j.saa.2025.127036 · Cited by 1
Volatile organic compound signatures in breast cancer: A pilot study on cell-based detection
Tenorio-Salazar, A. J., Orduña-Medina, F. M., Mizaikoff, B., Mitrovics, J., de León-Martínez, L. D., & Alcántara-Quintana, L. E. (2025) · Clinica Chimica Acta · doi:10.1016/j.cca.2025.120752 · Cited by 1
The environmental pollutant F-53B accelerates triple-negative breast cancer progression through metabolic reprogramming
Lao, S., Xie, J., Ou, Y., Liu, H., Fu, Q., Wu, J., Qin, L., Li, R., Zeng, K., Wang, S., et al. (2025) · Ecotoxicology and Environmental Safety · doi:10.1016/j.ecoenv.2025.119536 · Cited by 1
RAB10 mediates metabolic regulation of ferroptosis in breast Cancer and synergistically remodels the tumour immune microenvironment via macrophage M2 polarization
Li, R., Liu, Y., Pang, B., Liu, X., Zhu, C., Tang, G., Ran, R., Wang, W., Chen, C., & Yang, Q. (2026) · International Immunopharmacology · doi:10.1016/j.intimp.2026.116201 · Cited by 1
The miR-378a-3p/SLC7A11 axis mediates benzo[a]pyrene-induced ferroptosis in hippocampal neuronal cells
Wang, F., Shi, X., Gao, X., Li, D., Guo, Y., Chang, L. Y., & Wang, Y. (2026) · NeuroToxicology · doi:10.1016/j.neuro.2026.103406 · Cited by 1
A label-free microLC–SWATH-MS methodology with immunoaffinity depletion of highly abundant serum proteins for quantitative proteomic comparison of fresh-frozen human normal breast tissue and tumor clinical specimens
Macur, K., Bogucka, A. E., Fel, A., Skokowski, J., Ołdziej, S., & Czaplewska, P. (2026) · Frontiers in Molecular Biosciences · doi:10.3389/fmolb.2026.1739472 · Cited by 1
“…of processes related to amino acid and organic substance response reflects metabolic reprogramming, a hallmark of cancer and a defining feature of TNBC, which relies heavily on altered glycolysis, oxidative phosphorylation, and amino acid metabolism (Wang et al., 2020; Wei et al., 2021).”
Applications of Metabolomics to the Clinical Management of Breast Cancer: New Perspectives for Diagnosis, Treatment and Prognosis
Li, Y., & Mo, H. (2026) · International Journal of Molecular Sciences · doi:10.3390/ijms27052114 · Cited by 1
“…amino acid metabolism, lipid metabolism, and other branched pathways in triple-negative breast cancer (TNBC) fulfills bioenergetic and biosynthetic demands of tumor cells, maintains the redox balance, and further promotes oncogenic signaling, cell proliferation, and metastasis [23].”
Tumor-infiltrating lymphocytes in triple-negative breast cancer: molecular mechanisms, spatial regulation, and therapeutic implications
Li, Y., Li, Z., & Dai, J. (2026) · Breast Cancer Research · doi:10.1186/s13058-026-02285-w · Cited by 1
Live-Cell Optical Redox Imaging Reveals Metabolic Heterogeneity and Context-Dependent Responses to Metabolic Perturbation in TNBC Cells
Xu, H. N., Kollmar, J., Podsednik, A., Wannousse, M., Shestov, A., O’Connor, R. S., Baur, J. A., Tchou, J. C., Zhou, R., & Li, L. Z. (2026) · Metabolites · doi:10.3390/metabo16090613 · Cited by 1
“…however, they retain metabolic flexibility and can maintain or upregulate mitochondrial oxidative phosphorylation (OXPHOS) under conditions such as metastasis, cancer stemness, or metabolic stress, reflecting a context-dependent use of both glycolytic and mitochondrial pathways [9,12–14].”
Epigenetic Plasticity in Triple-Negative Breast Cancer: Mechanisms of Therapy Resistance, Biomarkers, and Therapeutic Vulnerabilities
Alaa, A. R., El-Din, S. A. B., Farrag, M. A., Ahmed, Y., Aziz, M. E. A., Abdel-Ghany, S. E., Arneth, B., & Sabit, H. (2026) · Biomedicines · doi:10.3390/biomedicines14092013 · Cited by 1
“This process provides lipids for building membranes and storing energy [79,80].”
The role of SRC-3 in prostate cancer progression and implications for therapeutic targeting: A systematic review
Zakari, S., Cleanclay, W. D., Bella-Omunagbe, M., Zakari, H., Ogbu, C. O., Uti, D. E., & Ogunlana, O. O. (2024) · Journal of Pharmacy & Pharmacognosy Research · doi:10.20944/preprints202310.0577.v1 · Cited by 1
Identification of TAT as a Biomarker Involved in Cell Cycle and DNA Repair in Breast Cancer
Xie, F., Hua, S., Guo, Y., Wang, T., Shan, C., Zhang, L., & He, T. (2024) · Biomolecules · doi:10.3390/biom14091088 · Cited by 1
“Glucose metabolism, amino acid metabolism, and fatty acid metabolism/amino acid metabolism in BC have been identified as critical factors in the metastasis and chemoresistance process of BC [6,7].”
Background
Genetic heterogeneity and metabolic reprogramming in breast cancer
Dolaş, Y., Buruş, A., & Çeltikçi, B. (2024) · Acta Medica · doi:10.32552/2024.actamedica.1060 · Cited by 1
Research progresses and hotspots on glucose metabolic reprogramming in breast cancer: a bibliometric analysis over the past two decades
Huang, L. H., Zhao, W., Sun, L., Niu, D., Zhu, X., & Jin, C. (2025) · Frontiers in Oncology · doi:10.3389/fonc.2024.1493996 · Cited by 1
“…the upregulation of glycolysis-related enzymes (e.g., hexokinase, pyruvate kinase, and phosphofructokinase) and transport proteins (e.g., glucose transporters and monocarboxylate transporters) in TNBC is associated with the activation of certain signaling pathways and transcription factors (20).”
Peptide-based drugs to inhibit LDH5, a potential target for cancer therapy
Nadal‐Bufí, F. (2022) · Queensland University of Technology · doi:10.5204/thesis.eprints.232526 · Cited by 1
Recurrent triple-negative breast cancer from cysteine deprivation loses tumorigenicity via downregulation of the CST4 signalingPreprint
Tang, X., Alothaim, T., & Charbonneau, M. (2022) · Research Square · doi:10.21203/rs.3.rs-1943456/v1 · Cited by 1
PFKP Accelerates Malignant Features in Breast CancerPreprint
Shibata, M., Inaishi, T., Ichikawa, T., Kanda, M., Hayashi, M., Soeda, I., Takeuchi, D., Takano, Y., Tsunoda, N., Kodera, Y., et al. (2021) · Research Square · doi:10.21203/rs.3.rs-258864/v1
Quantitative and visualized analysis of 5,097 triple-negative breast cancer (TNBC) publications by using multiple machine learning algorithms: TNBC is an excellent forerunner in cancer researchPreprint
Wang, K., Zheng, C., Xue, L., Deng, D., Tan, F., Pei, Q., Li, Y., Wang, D., Zeng, L., Li, M., et al. (2021) · Research Square · doi:10.21203/rs.3.rs-783425/v1
Integrated Metabolic and Gene Expression Profiling Reveals New Therapeutic Modalities for Rapidly Proliferating Breast CancersPreprint
Liao, C., Glodowski, C. R., Fan, C., Liu, J., Mott, K. R., Kaushik, A., Vu, H. S., Locasale, J. W., McBrayer, S. K., DeBerardinis, R. J., et al. (2021) · Research Square · doi:10.21203/rs.3.rs-117384/v2
MicroRNA-612 regulates the proliferation and epithelial-to-mesenchymal transition of human colon cancer cells via G protein-coupled receptor 132 (GPR132)
Shen, S., Guo, Q., & Zhan, S. (2022) · Tropical Journal of Pharmaceutical Research · doi:10.4314/tjpr.v20i7.4
ATP5b and Bioenergetic Plasticity in Breast Cancer Metastasis and Tumour Microenvironment Interactions
Lewthwaite, D. (2023) · doi:10.26686/wgtn.23787291
Single-cell RNA sequencing has unveiled the contribution of ADSCs in reprogramming metabolism in triple-negative breast cancerPreprint
Zhang, L., Xiao, Q., Zhang, M., Liu, X., & Zhou, L. (2024) · Research Square · doi:10.21203/rs.3.rs-3893986/v1
Identification of Key Therapeutic Targets of Triptolide Against Breast Cancer by Integrated Transcriptomic Analysis and Co-expression Network ApproachPreprint
Luo, Y., Xing, J., Wang, C., Yingqiu, W., Zhang, L., & Hongwei, L. (2024) · Research Square · doi:10.21203/rs.3.rs-3992734/v1
Investigação de moduladores da tubulina com propriedades anticâncer
Souza, M. D. S. (2024) · Digital Library of Theses and Dissertations (Universidade de São Paulo) · doi:10.11606/t.76.2024.tde-18062024-093531
Insular/perisylvian epilepsy: Open resection versus stereotactic ablation (MR-guided laser ablation/radiofrequency thermocoagulation) versus responsive neurostimulation
Joris, V., Royer, J., & Weil, A. G. (2024) · Elsevier eBooks · doi:10.1016/b978-0-323-95981-0.00004-7

Authors: Wang, Z., Jiang, Q., & Dong, C.
Affiliations: Second Affiliated Hospital of Zhejiang University (CN)
Zhejiang University (CN)
Corresponding author: Dong, Chenfang
ORCID: Wang, Zhanyu
Dong, Chenfang
Venue: Cancer Biology and Medicine
Publisher: China Anti-cancer Association
Published: 2020
Volume: 17
Issue: 1
Pages: 44-59
ISSN: 2095-3941 (ISSN-L)
DOI: 10.20892/j.issn.2095-3941.2019.0210
PMC: PMC7142847
OpenAlex: W3020548503
Cited by: 248
References: 135
Citations by year: 2026: 61 · 2025: 63 · 2024: 46 · 2023: 31 · 2022: 20 · 2021: 18 · 2020: 8
FWCI: 6.58
Type: journal article
Language: en
Open access: gold
doi.org
Licence: cc-by
Locations: Cancer Biology and Medicine (publishedVersion, cc-by)
PubMed Central (publishedVersion, cc-by)
PubMed (publishedVersion)
DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Hypoxia, and Metabolism
Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Lipids, and Metabolism
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
Keywords: triple-negative breast cancer, metabolic reprogramming, glycolysis, oxidative phosphorylation, amino acid metabolism, lipid metabolism, redox homeostasis, oncogenic signaling, metastasis, metabolic biomarkers, metabolic imaging
MeSH terms: Warburg Effect, Oncologic, Amino Acids, Antineoplastic Agents, Female, Humans, Oxidative Phosphorylation, Biomarkers, Tumor, Lipid Metabolism, Molecular Targeted Therapy, Triple Negative Breast Neoplasms

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review

Metabolic reprogramming in triple-negative breast cancer

Abstract

Overview

Integrity signals

Figures

Verification

Claims the paper makes

Claims other papers make about this one

Self-check

Citations

Cites

Cited by

Related

Metadata

Record

About these checks