Role of hypoxia inducible factor-1 in cancer stem cells (Review)

• Published in: Molecular medicine reports Vol. 23; no. 1; p. 1
• Main Authors: Zhang, Qi, Han, Zhenzhen, Zhu, Yanbo, Chen, Jingcheng, Li, Wei
• Format: Journal Article
• Language: English
• Published: Greece Spandidos Publications 01.01.2021; Spandidos Publications UK Ltd; D.A. Spandidos
• Subjects: Apoptosis; Binding sites; Biomarkers, Tumor - metabolism; Breast cancer; Cancer; Cancer cells; Carcinogenesis; Cell adhesion & migration; Cell cycle; Cell growth; Cell self-renewal; Colorectal cancer; Deoxyribonucleic acid; DNA; DNA methylation; Epigenetics; Epithelial-Mesenchymal Transition; Ewings sarcoma; Gastric cancer; Gene expression; Gene Expression Regulation, Neoplastic; Genetic aspects; Health aspects; Humans; Hypoxia; Hypoxia-inducible factor 1; Hypoxia-Inducible Factor 1 - metabolism; Kinases; Liver cancer; Lung cancer; Medical prognosis; Mesenchyme; Metastases; Metastasis; MicroRNAs; Neoplasms - metabolism; Neoplastic Stem Cells - metabolism; Non-coding RNA; Phosphorylation; Proteins; Radiation therapy; Review; Stem cells; Transcription factors; Tumor Microenvironment; China
• ISSN: 1791-2997; 1791-3004
• DOI: 10.3892/mmr.2020.11655

Cancer stem cells (CSCs) have been found to play a decisive role in cancer recurrence, metastasis, and chemo‑, radio‑ and immuno‑resistance. Understanding the mechanism of CSC self‑renewal and proliferation may help overcome the limitations of clinical treatment. The microenvironment of tumor growth consists of a lack of oxygen, and hypoxia has been confirmed to induce cancer cell invasion, metastasis and epithelial‑mesenchymal transition, and is usually associated with poor prognosis and low survival rates. Hypoxia inducible factor‑1 (HIF‑1) can be stably expressed under hypoxia and act as an important molecule to regulate the development of CSCs, but the specific mechanism remains unclear. The present review attempted to explain the role of HIF‑1 in the generation and maintenance of CSCs from the perspective of epigenetics, metabolic reprogramming, tumor immunity, CSC markers, non‑coding RNA and signaling pathways associated with HIF‑1, in order to provide novel targets with HIF‑1 as the core for clinical treatment, and extend the life of patients.