The deubiquitinase USP10 protects pancreatic cancer cells from endoplasmic reticulum stress

被引：0
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作者：
Udayan Bhattacharya
Elangovan Thavathiru
Fiifi Neizer-Ashun
Chao Xu
Zoran Gatalica
Shailendra Kumar Dhar Dwivedi
Anindya Dey
Priyabrata Mukherjee
Resham Bhattacharya
机构：
[1] University of Oklahoma Health Sciences Center,Department of Obstetrics and Gynecology
[2] University of Oklahoma Health Sciences Center,Department of Cell Biology
[3] University of Oklahoma Health Sciences Center,Department of Biostatistics and Epidemiology
[4] University of Oklahoma Health Sciences Center,Department of Pathology
[5] University of Oklahoma Health Sciences Center,Peggy and Charles Stephenson Cancer Center
来源：
npj Precision Oncology | / 6卷
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摘要：
The ubiquitin-specific peptidase 10 (USP10) plays a context-specific, pro or anti-tumorigenic role in different malignancies. However, the role of USP10 in pancreatic cancer remains unclear. Our protein and RNA level analysis from archived specimens and public databases show that USP10 is overexpressed in pancreatic ductal adenocarcinoma (PDAC) and expression correlates with poor overall patient survival. Phenotypically, silencing USP10 decreased viability, clonal growth and invasive properties of pancreatic cancer cells. Mechanistically, silencing USP10 upregulated BiP and induced endoplasmic reticulum (ER) stress that led to an unfolded protein response (UPR) and upregulation of PERK, IRE1α. Decreased cell viability of USP10 silenced cells could be rescued by a chemical chaperone that promotes protein folding. Our studies suggest that USP10 by protecting pancreatic cancer cells from ER stress may support tumor progression.
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