Radiation activates HIF-1 to regulate vascular radiosensitivity in tumors: role of reoxygenation, free radicals, and stress granules.

By B. Moeller, Yiting Cao, Chuan-Yuan Li, Mark W. Dewhirst. Cancer Cell, 2004

998 citations recorded by the source corpus.

Subfields: Cancer Research, Molecular Biology, Radiology, Nuclear Medicine and Imaging

View Paper: https://www.semanticscholar.org/paper/5b4f85899af1a04615a41e195e4c479103692e05

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Citations in the corpus

Caspase 3-mediated stimulation of tumor cell repopulation during cancer radiotherapy (2011, positive): “For example, radiation-induced up-regulation of angiogenic activities in tumors has been linked with activation of upstream transcriptional factors such as HIF-1 6 .”
Therapeutic targeting of hypoxia and hypoxia-inducible factors in cancer. (2016, background): “ROS production later stabilizes the HIF-1α protein and increases expression of HIF-1α and its target genes (Moeller et al., 2004; Dewhirst et al., 2008; Harada et al., 2009).”
Eukaryotic stress granules: the ins and outs of translation. (2009, background): “Some specific mRNAs are inefficiently repressed when RNA-binding proteins that contribute to stress granule formation are altered (Moeller et al., 2004; Kedersha et al., 2000; Gilks et al., 2004; Tsai et al., 2008; Mazroui et al., 2007), but these effects may simply reflect loss of a specific mRNP…”
Defining the Role of Hypoxia-Inducible Factor 1 in Cancer Biology and Therapeutics (2009, neutral): “Radiation was shown to induce HIF-1 activity, leading to the production of VEGF and other angiogenic cytokines that protect the endothelial cells of the tumor vasculature from radiation-induced death (Moeller et al., 2004).”
Digoxin and other cardiac glycosides inhibit HIF-1α synthesis and block tumor growth (2008, neutral): “Exposure of cancer cells to hypoxia induces the formation of stress granules containing mRNAs that are not translated until the cells are reoxygenated (37).”
Oxygen sensing requires mitochondrial ROS but not oxidative phosphorylation. (2005, background): “radiation-induced reoxygenation of hypoxic tumor cells results in the production of ROS, which activates HIF-1 to prevent radiation-induced endothelial cell death (Moeller et al., 2004).”
Hypoxic microenvironment in cancer: molecular mechanisms and therapeutic interventions (2023, background): “Radiation upregulates HIF-1 expression and enhances its activity in cancer cells.(381) Elevated HIF-1α levels confer radioresistance via various pro-cancer mechanisms.”
Hypoxia-inducible factors in stem cells and cancer (2009, neutral): “Similar to the case of cMyc, the effects of HIF on p53 can be context-dependent [99,101].”
The role of hypoxia-inducible factors in tumorigenesis (2008, background): “through the release of proangiogenic cytokines such as VEGF.(102) In contrast, HIF-1 can also induce tumor radiosensitivity through the induction of apoptosis.”
The interaction of anticancer therapies with tumor-associated macrophages (2015, background): “Recruitment of macrophages ultimately leads to tumor recurrence (Moeller et al., 2004; Shiao and Coussens, 2010; Moding et al., 2013; Russell and Brown, 2013; Xu et al., 2013).”
HIF-1 mediates adaptation to hypoxia by actively downregulating mitochondrial oxygen consumption. (2006, background): “Current tumor models suggest that inhibiting HIF target genes such as VEGF will reduce tumor angiogenesis (Moeller et al., 2004).”