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Mol Cell Oncol. 2015 Apr 14;2(4):e1030537. doi: 10.1080/23723556.2015.1030537. eCollection 2015 Oct-Dec.

HIGD1A-mediated dormancy and tumor survival.

Author information

1
Department of Pediatrics; University of California, San Francisco ; San Francisco, CA, USA.
2
Department of Pediatrics; University of California, San Francisco; San Francisco, CA, USA; Department of Biomedical Sciences; University of California, San Francisco; San Francisco, CA, USA; Department of Developmental and Stem Cell Biology; University of California, San Francisco; San Francisco, CA, USA.

Abstract

Solid tumors contain regions of anoxia that are also glucose deprived. How cancer cells survive such extreme conditions remains unclear. Here, we discuss our recent findings that regulation of hypoxia inducible gene domain family member 1 A (HIGD1A) via epigenetic mechanisms during glucose starvation modulates oxygen consumption and reactive oxygen species production to enable tumor cell survival through the activation of dormancy mechanisms.

KEYWORDS:

AMPK; DNMT1; HIF; glucose deprivation; hypoxia; tumor dormancy

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