Regulation of HIFs in Cancer Cells
A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Tumor Microenvironment".
Deadline for manuscript submissions: closed (31 October 2024) | Viewed by 6050
Special Issue Editors
Interests: Hypoxia; Hypoxia-inducible Factors (HIFs); HIF-2 regulation and post-translational modifications; cell signaling in cancer cells; oxidative stress; endothelium; angiogenesis
Interests: Hypoxia; Hypoxia-inducible factor-1 (HIF-1); regulation of gene expression; cell signaling and cancer; nucleocytoplasmic transport; nuclear structure and function; regulation of lipid metabolism
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Special Issue Information
Dear Colleagues,
Hypoxia, a condition in which cells are exposed to reduced oxygen levels, is implicated in physiological processes, such as life in high altitude and intense exercise, but also in pathologic conditions, including ischemia, inflammatory disorders, pulmonary diseases, renal diseases, and cancer. Cancer cells under hypoxia exhibit significant changes in gene expression patterns in order to facilitate their adaptation under the hypoxic microenvironment. This transcriptional reprogramming is mainly coordinated by Hypoxia-Inducible transcription Factors (HIF) and allows cells to alter their metabolism, proliferate, and acquire resistance to death. However, it also facilitates processes such as angiogenesis and vascularization of the tumor, invasion, and metastasis.
HIFs are a small family of heterodimeric transcription factors comprising three distinct isoforms (HIF-1, HIF-2, HIF-3), and consist of an oxygen-regulated HIF-α subunit and a stably expressed HIF-β subunit or ARNT (Aryl hydrocarbon Receptor Nuclear Translocator). HIF-α oxygen-regulated subunits are often overexpressed in human cancers, not only by local hypoxia but also by oncogenic mutations (as in VHL) or overactivation of signaling pathways such as PI3K/AKT/mTOR or Ras/ERK1/2 that stimulate HIF-α expression and/or HIF transcriptional activity. In addition, the overexpression of HIF-α is observed in many cancers and is strongly correlated with poor patient prognosis and resistance to conventional therapy.
Thus, HIFs represent an attractive target for anticancer therapy and a global effort is underway to find strategies to control and modulate HIF activity for therapeutic purposes. Recent preclinical models and clinical studies have shown the prospects of inhibiting HIF in poorly oxygenated cancer cells; however, the full potential of HIF inhibition may be revealed when it is combined with other treatments as a tool to fight cancer.
Therefore, in order to develop new tools that effectively impact hypoxic cancer cells and limit tumor growth, it is important to elucidate the mechanistic details of HIF regulation in cancer cells and gain new knowledge on the contribution of various HIF isoforms in different types of cancer.
Dr. Panagiotis Liakos
Dr. Ilias Mylonis
Guest Editors
Manuscript Submission Information
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Keywords
- Hypoxia
- Hypoxia-inducible Factors (HIFs)
- tumor microenvironment
- cancer
- oxygen
- transcription
- post-translational modifications
- mRNA synthesis
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