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NDRG 2 acts as a PERK co‐factor to facilitate PERK branch and ERS ‐induced cell death
Author(s) -
Zhang Mei,
Liu Xiping,
Wang Qinhao,
Ru Yi,
Xiong Xin,
Wu Kaichun,
Yao Libo,
Li Xia
Publication year - 2017
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1002/1873-3468.12861
Subject(s) - computer network , computer science
NDRG 2 , a newly identified tumor suppressor, is also responsive to various stresses, such as hypoxia and DNA damage. Here, we reported that in human hepatoma SK ‐Hep‐1 and HepG2 cells, NDRG 2 mRNA and protein levels were upregulated by different endoplasmic reticulum stress inducers including Tg, Tm, and DTT. Further, using NDRG 2‐overexpressing hepatoma cell lines and Ndrg2 KO mice liver tissues, we found that, among the three branches of unfolded protein response signaling, NDRG 2 facilitates protein kinase RNA‐like ER kinase ( PERK ) pathway via interaction with PERK , enhancing its downstream ATF 4 and CHOP . Functionally, NDRG 2 promotes ERS ‐induced apoptosis partially through ATF 4 or CHOP . Thus, NDRG 2 is a novel ERS ‐responsive protein and acts as PERK co‐factor to facilitate PERK branch, thereby contributing to ERS ‐induced apoptosis.