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USP32 promotes tumorigenesis and chemoresistance in gastric carcinoma via upregulation of SMAD2 by Dou, Ning; Hu, Qingqing; Li, Li; Wu, Qiong; Li, Yandong; Gao, Yong is a Biochemistry, Genetics and Molecular Biology article available to read on EtoBox.

What is USP32 promotes tumorigenesis and chemoresistance in gastric carcinoma via upregulation of SMAD2 about?

USP32, a member of the ubiquitin-specific proteases family, has been implicated in the development of breast cancer and small lung cancer. However, its biological functions and clinical significance in gastric cancer (GC) remain unclear. In the present study, we reported that knockdown or depletion of USP32 significantly inhibited GC cell proliferation and migration __in vitro__ and __in vivo,__ indicating that USP32 functions as an oncogene in GC. Importantly, results from immunohistochemical staining in a tissue microarray revealed that USP32 was upregulated in GC tissues compared with paracancerous tissues. Further analyses showed that high expression of USP32 was closely related with high T-staging and poor outcomes of GC patients. Mechanistically, USP32 silencing caused a decrease in the expression of SMAD2, which resulted in the inhibitory effects of GC cells on growth, motility, and chemoresistance to cisplatin. Therefore, our findings strongly suggest the involvement of USP32 in GC progression and provide a potential target for future therapy of GC.

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Author

Dou, Ning; Hu, Qingqing; Li, Li; Wu, Qiong; Li, Yandong; Gao, Yong

Publisher

Ivyspring International Publisher; Bluehaven (N.S.W.): Ivyspring International, 2004- (ISSN 1449-2288)

Published

2020

Language

EN

Field

Biochemistry, Genetics and Molecular Biology (Life Sciences)