The DOI matches its Crossref record; 136 of the 136 references it cites were found in a registry or an index.
Hypoxia: Overview on Hypoxia-Mediated Mechanisms with a Focus on the Role of HIF Genes
Open accessAbstract
Hypoxia represents a frequent player in a number of malignancies, contributing to the development of the neoplastic disease. This review will discuss the means by which hypoxia powers the mechanisms behind cancer progression, with a majority of examples from lung cancer, the leading malignancy in terms of incidence and mortality rates (the frequent reference toward lung cancer is also for simplification purposes and follow up of the global mechanism in the context of a disease). The effects induced by low oxygen levels are orchestrated by hypoxia-inducible factors (HIFs) which regulate the expression of numerous genes involved in cancer progression. Hypoxia induces epithelial-to-mesenchymal transition (EMT) and metastasis through a complex machinery, by mediating various pathways such as TGF-β, PI3k/Akt, Wnt, and Jagged/Notch. Concomitantly, hypoxic environment has a vast implication in angiogenesis by stimulating vessel growth through the HIF-1α/VEGF axis. Low levels of oxygen can also promote the process through several other secondary factors, including ANGPT2, FGF, and HGF. Metabolic adaptations caused by hypoxia include the Warburg effect—a metabolic switch to glycolysis—and GLUT1 overexpression. The switch is achieved by directly increasing the expression of numerous glycolytic enzymes that are isoforms of those found in non-malignant cells.
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Cites
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Targeting HIF-1 for cancer therapy
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“However, none of these small molecules were designed for specific targeting of HIF-1α, fact that hampers the translational switch toward the patients due to difficulties in controlling the level of action and selection of the targeted cohort [137].”
BackgroundOverview of MicroRNA Biogenesis, Mechanisms of Actions, and Circulation
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The tumour suppressor protein VHL targets hypoxia-inducible factors for oxygen-dependent proteolysis
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Targeting Hypoxia-Inducible Factors for the Treatment of Anemia in Chronic Kidney Disease Patients
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“HIF-1, the hypoxic master regulator, binds to the HRE in the promoter region of the key driving entity in angiogenesis—VEGF [84].”
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Cited by
Hypoxia signaling in human health and diseases: implications and prospects for therapeutics
Luo, Z., Tian, M., Yang, G., Tan, Q., Chen, Y., Li, G., Zhang, Q., Li, Y., Wan, P., & Wu, J. (2022) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-022-01080-1 · Cited by 499
Mesenchymal stem cells: Amazing remedies for bone and cartilage defects
Kangari, P., Talaei-Khozani, T., Razeghian-Jahromi, I., & Razmkhah, M. (2020) · Stem Cell Research & Therapy · doi:10.1186/s13287-020-02001-1 · Cited by 286
Emerging role of tumor cell plasticity in modifying therapeutic response
Qin, S., Jiang, J., Lu, Y., Nice, E. C., Huang, C., Zhang, J., & He, W. (2020) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-020-00313-5 · Cited by 268
Tumor cell plasticity in targeted therapy-induced resistance: Mechanisms and new strategies
Shi, Z.-D., Pang, K., Wu, Z.-X., Dong, Y., Hao, L., Qin, J.-X., Wang, W., Chen, Z.-S., & Han, C.-H. (2023) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-023-01383-x · Cited by 256
Metadata
- Authors
- Tirpe, A. A., Gulei, D., Ciortea, S. M., Crivii, C., & Berindan-Neagoe, I.
- Venue
- International Journal of Molecular Sciences
- Publisher
- MDPI AG
- Published
- 2019-12-05
- Volume
- 20
- Issue
- 24
- Pages
- 6140
- ISSN
- 1422-0067 (ISSN-L)
- OpenAlex
- W2992297284
- Cited by
- 438
- References
- 136
- FWCI
- 14.03
- Type
- journal article
- Language
- en
- Open access
- gold
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- Tirpe, A. A., Gulei, D., Ciortea, S. M., Crivii, C., & Berindan-Neagoe, I. (2019). Hypoxia: Overview on Hypoxia-Mediated Mechanisms with a Focus on the Role of HIF Genes. International Journal of Molecular Sciences. https://doi.org/10.3390/ijms20246140
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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