Molecular mechanism of triple‑negative breast cancer‑associated BRCA1 and the identification of signaling pathways
Open accessAbstract
BRAC1 has multiple important interactions with triple-negative breast cancer, the specific molecular characteristics of this interaction, however, have not yet been completely elucidated. By examining cell signaling pathways, important information for comprehending the potential mechanisms of this cancer may become known. The aim of the present study was to identify the effects of BRAC1 and to find the signaling pathway(s) involved in the pathogenic mechanism of triple-negative breast cancer. In this study, GSE27447 microarray data were obtained from the Gene Expression Omnibus (GEO) database of the National Center for Biotechnology Information, and differentially expressed genes (DEGs) from GSE27447 were distinguished by Significant Analysis of Microarray. Gene ontology (GO) analysis was carried out on 132 upregulated and 198 downregulated genes with DAVID. The signaling was forecast by the Kyoto Encyclopedia of Genes and Genomes (KEGG). Transcription factors were recognized by TFatS. The BRAC1 relevant protein-protein interaction networks (PPI) were fixed by STRING and visualized by CytoScape. Overall, the upregulated DEGs, which included CR2, IGHM, PRKCB, CARD11, PLCG2, CD79A, IGKC and CD27, were primarily enriched in the terms associated with immune responses, and the downregulated DEGs, which included STARD3, ALDH8A1, SRD5A3, CACNA1H, UGT2B4, SDR16C5 and MED1, were primarily enriched in the hormone metabolic process. In addition, 13 pathways, such as the B-cell receptor-signaling pathway, the hormone synthesis signaling pathway and the oxytocin-signaling pathway, were chosen. MYC, SP1 and CTNNB1 were determined to be enriched in triple-negative breast cancer. A total of 8 genes were identified to be downregulated in the BRAC1-related PPI network. The results of the present study show a fresh angle on the molecular mechanism of triple-negative breast cancer and indicate a possible target for its treatment.
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PLCγ2 was upregulated and potentially involved in triple-negative breast cancer-associated BRAC1 in a Chinese patient cohort.
“Population studies and microarray analyses also revealed PLCγ2 associated with the EGFR pathway was a risk factor in esophageal squamous cell carcinoma and gastric cancer (149), in non–small-cell lung cancer associated with HMGB1 expression (150), and as upregulated and potentially involved in triple-negative breast cancer–associated BRAC1 in a Chinese patient cohort (151).”
From The role of PLCγ2 in immunological disorders, cancer, and neurodegeneration (2021) · cites this paper as [151]
The Abstract lists PLCG2 among upregulated genes, and 'Verifying the expression of DEGs and transcription factors' reports increased PLCG2 expression in TNBC patient samples. The Patient samples section places the small validation sample at a Shanghai hospital and diagnostic center, but does not establish the patients’ nationality. The BRCA1-associated PPI network section says no proteins encoded by upregulated genes interacted with BRCA1, so the paper does not establish a PLCG2–BRCA1 interaction. (LLM, conf=0.85)
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Targeting ERα36: A Promising Strategy for Treating Triple-Negative Breast Cancer
Banu, Z. W., Das, A., Patowary, L., Ahmed, N., Kushari, S., Sarma, K., Borgohain, R., & Kalita, J. M. (2026) · Current Cancer Therapy Reviews · doi:10.2174/0115733947389267251110045959
- Authors
- Qi, F., Qin, W., & Zang, Y.
- Affiliations
- Second Military Medical University (CN)
- Department of Oncology, Changzheng Hospital, Second Military Medical University, Shanghai 200003, P.R. China
- ORCID
- Zang, Yuan‑Sheng
- Venue
- Oncology Letters
- Publisher
- Spandidos Publications
- Published
- 2019-01-03
- Volume
- 17
- Issue
- 3
- Pages
- 2905-2914
- ISSN
- 1792-1074 (ISSN-L)
- 1792-1082
- PMC
- PMC6365902
- OpenAlex
- W2907775063
- Cited by
- 32
- References
- 66
- Citations by year
- 2026: 2 · 2024: 7 · 2023: 3 · 2022: 8 · 2021: 6 · 2020: 5 · 2019: 1
- FWCI
- 1.58
- Type
- journal article
- Language
- en
- Open access
- diamond
- doi.org
- Locations
- Oncology Letters (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Natural Science Foundation of China (81502260)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Breast Cancer Treatment Studies
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › BRCA gene mutations in cancer
- Health Sciences › Medicine › Pathology and Forensic Medicine › Breast Lesions and Carcinomas
- Keywords
- triple-negative breast cancer, BRCA1, signaling pathways, differentially expressed genes, B cell receptor signaling, oxytocin signaling pathway, protein-protein interaction network, c-Myc, Sp1, CTNNB1, immune response genes, therapeutic target
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.
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