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Cancer Lett. 2015 Sep 1;365(2):201-10. doi: 10.1016/j.canlet.2015.05.027. Epub 2015 Jun 3.

IDH1, a CHOP and C/EBPβ-responsive gene under ER stress, sensitizes human melanoma cells to hypoxia-induced apoptosis.

Author information

1
Institute of Cancer Stem Cell, Second Affiliated Hospital, Dalian Medical University, Dalian 116044, China.
2
Department of Immunology, Anhui Medical University, Hefei, Anhui 230601, China.
3
Oncology Department, The Second Hospital of Anhui Medical University, Hefei, Anhui 230601, China. Electronic address: bluelin523@163.com.
4
Institute of Cancer Stem Cell, Second Affiliated Hospital, Dalian Medical University, Dalian 116044, China. Electronic address: hanchuanchun@163.com.

Abstract

Isocitrate dehydrogenase1 (IDH1) is of great importance in cell metabolism and energy conversion. However, alterations in IDH1 in response to stress and excise-regulated mechanisms are not well described. Here we investigated gene expression profiles under ER stress in melanoma cells and found that IDH1 was dramatically increased with ER stress induced by tunicamycin. Elevated IDH1 subsequently sensitized human melanoma cells to hypoxia-induced apoptosis and promoted HIF-1α degradation. In addition, we revealed that CHOP and C/EBPβ were involved in hypoxia-induced apoptosis via transcriptional regulation of IDH1 expression. Our data indicate that IDH1, regulated by CHOP and C/EBPβ in response to ER stress treatment, inhibits survival of melanoma cells under hypoxia and promotes HIF-1α degradation. Therefore, we propose that IDH1 may serve as a valuable target for melanoma therapy.

KEYWORDS:

Apoptosis; CHOP; ER stress; HIF-1α; IDH1

PMID:
26049021
DOI:
10.1016/j.canlet.2015.05.027
[Indexed for MEDLINE]

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