USP28 promotes aerobic glycolysis of colorectal cancer by increasing stability of FOXC1

被引：13

作者：

Liu, Zhaohui ^{[1
]}

Chen, Min ^{[2
]}

Xu, Xiaoping ^{[1
]}

Zhang, Lei ^{[1
]}

Pan, Yuan ^{[1
]}

Chen, Dong ^{[1
]}

机构：

[1] First Peoples Hosp Yuhang Dist, Dept Anorectal Surg, Hangzhou 311100, Zhejiang, Peoples R China

[2] First Peoples Hosp Yuhang Dist, Dept Anesthesia, Hangzhou 311100, Zhejiang, Peoples R China

来源：

ACTA BIOCHIMICA POLONICA | 2021年 / 68卷 / 04期

关键词：

USP28; FOXC1; aerobic glycolysis; stability; colorectal can-cer; INTESTINAL HOMEOSTASIS; C-MYC; METABOLISM; CELLS; FBW7;

D O I：

10.18388/abp.2020_5504

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Aerobic glycolysis is essential for cancer cell metabolism and growth. Deubiquitinase, USP28 (ubiquitin specific peptidase 28), could maintain stability of proteins in-volved in tumor progression. This study was performed to investigate the role of USP28 in aerobic glycolysis of colorectal cancer. Our data showed that USP28 mRNA and protein expressions were enhanced in colorectal cancer tissues and cells. Functional assays demonstrated that overexpression of USP28 promoted cell proliferation and aerobic glycolysis of colorectal cancer, while USP28 inhibition could reverse these effects. Protein expression of Forkhead Box C1 (FOXC1) was increased by USP28 over-expression, whereas knockdown of USP28 aggra-vated cycloheximide (CHX; protein synthesis inhibitor) stimulated decrease of FOXC1. Moreover, proteasome inhibitor, MG132, could rescue USP28 silence-induced degradation of FOXC1. Overexpression of FOXC1 coun-teracted the suppressive effects of USP28 interference on colorectal cancer cell viability and aerobic glycolysis. In conclusion, USP28 enhanced cell viability and aerobic glycolysis of colorectal cancer by stabilizing FOXC1, sug-gesting that USP28-FOXC1 might be a novel therapeutic avenue for colorectal cancer.

引用

页码：633 / 639

页数：7

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