PRKCSH contributes to tumorigenesis by selective boosting of IRE1 signaling pathway

Gu-Choul Shin (), Sung Ung Moon, Hong Seok Kang, Hyo-Sun Choi, Hee Dong Han and Kyun-Hwan Kim ()
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Gu-Choul Shin: Konkuk University
Sung Ung Moon: Sookmyung Women’s University
Hong Seok Kang: Konkuk University
Hyo-Sun Choi: Konkuk University
Hee Dong Han: School of Medicine, Konkuk University
Kyun-Hwan Kim: Konkuk University

Nature Communications, 2019, vol. 10, issue 1, 1-16

Abstract: Abstract Unfolded protein response (UPR) is an adaptive mechanism that aims at restoring ER homeostasis under severe environmental stress. Malignant cells are resistant to environmental stress, which is largely due to an activated UPR. However, the molecular mechanisms by which different UPR branches are selectively controlled in tumor cells are not clearly understood. Here, we provide evidence that PRKCSH, previously known as glucosidase II beta subunit, functions as a regulator for selective activation of the IRE1α branch of UPR. PRKCSH boosts ER stress–mediated autophosphorylation and oligomerization of IRE1α through mutual interaction. PRKCSH contributes to the induction of tumor-promoting factors and to tumor resistance to ER stress. Increased levels of PRKCSH in various tumor tissues are positively correlated with the expression of XBP1-target genes. Taken together, our data provide a molecular rationale for selective activation of the IRE1α branch in tumors and adaptation of tumor cells to severe environmental stress.

Date: 2019
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DOI: 10.1038/s41467-019-11019-w

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