Special Issue "Gene Regulation by HIFs during Hypoxia"

A special issue of Cells (ISSN 2073-4409).

Deadline for manuscript submissions: 31 December 2018

Special Issue Editor

Guest Editor
Prof. George Simos

Laboratory of Biochemistry, Faculty of Medicine, University of Thessaly, Panepistimiou 3, BIOPOLIS, 41500 Larissa, Greece
Website | E-Mail
Interests: hypoxia; HIF-1; metabolism; phosphorylation; nuclear transport; cancer; apoptosis

Special Issue Information

Dear Colleagues,

Exposure of human cells and/or tissues to low oxygen conditions, which is termed hypoxia, characterizes healthy activities, such as intense muscular exercise and living at high altitudes, as well as many pathological conditions, including pulmonary diseases, ischemia, inflammatory disorders and cancer. Adaptation to hypoxic conditions requires dramatic changes in gene expression, orchestrated by the hypoxia inducible transcription factors HIF-1 and HIF-2.

Since the first break-through identification of HIF-1 in 1995 by Semenza and co-workers, we have learned a great deal, both about the mechanisms that regulate HIFs in response to oxygen concentration changes, and about HIF target genes, the products of which mediate metabolic reprogramming, angiogenesis, erythropoiesis and many other homeostatic changes that allow adaptation to hypoxia or lead to apoptosis and cell death under extreme lack of oxygen. These findings have established HIFs as major players in both health and disease and triggered a world-wide effort to find ways of controlling their activity for therapeutic purposes.

Investigations of single gene expression as well as genome-wide studies have shown that HIFs bind to a short consensus sequence termed Hypoxia Response Element (HRE). However, HREs are much more abundant in the human genome than the number of true HIF gene targets, making their prediction impossible and necessitating non-trivial experimental verification. In this respect, characterization of the genes directly regulated by hypoxia is an ongoing process, which continues to provide important information on the cellular pathways affected by hypoxia and their role in the hypoxic response. As drugs that target HIFs either as inhibitors, in the case of cancer, or as stimulants, in the case of defective erythropoiesis, have recently been developed and may soon enter the market, it becomes imperative to produce a full inventory of the genes, the expression of which is affected when HIF activity is modulated by medicinal agents.

Furthermore, the molecular/structural details and tissue or isoform specificity of the oxygen-dependent and oxygen-independent mechanisms that fine-tune HIF activity, control the choice of common or distinct HIF targets and affect the interaction of HIFs with chromatin and the transcriptional machinery are still a matter of intense investigation. Full delineation of these mechanisms and their spatio-temporal coordination can offer additional possibilities to artificially influence HIF-dependent gene expression as means for treating a disease.

Prof. George Simos
Guest Editor

Manuscript Submission Information

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Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 1000 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • hypoxia
  • HIF
  • chromatin
  • transcription
  • cancer
  • oxygen
  • metabolism
  • erythropoiesis

Published Papers (1 paper)

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Research

Open AccessArticle TNFSF14/LIGHT, a Non-Canonical NF-κB Stimulus, Induces the HIF Pathway
Received: 29 June 2018 / Revised: 6 August 2018 / Accepted: 7 August 2018 / Published: 8 August 2018
PDF Full-text (2072 KB) | HTML Full-text | XML Full-text | Supplementary Files
Abstract
Non-canonical NF-κB signalling plays important roles in the development and function of the immune system but it also is deregulated in a number of inflammatory diseases. Although, NF-κB and HIF crosstalk has been documented, this has only been described following canonical NF-κB stimulation,
[...] Read more.
Non-canonical NF-κB signalling plays important roles in the development and function of the immune system but it also is deregulated in a number of inflammatory diseases. Although, NF-κB and HIF crosstalk has been documented, this has only been described following canonical NF-κB stimulation, involving RelA/p50 and the HIF-1 dimer. Here, we report that the non-canonical inducer TNFSF14/LIGHT leads to HIF induction and activation in cancer cells. We demonstrate that only HIF-2α is induced at the transcriptional level following non-canonical NF-κB activation, via a mechanism that is dependent on the p52 subunit. Furthermore, we demonstrate that p52 can bind to the HIF-2α promoter in cells. These results indicate that non-canonical NF-κB can lead to HIF signalling implicating HIF-2α as one of the downstream effectors of this pathway in cells. Full article
(This article belongs to the Special Issue Gene Regulation by HIFs during Hypoxia)
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