PIK3R3 inhibits cell senescence through p53/p21 signaling

被引：41

作者：

Chen, Qianzhi ^{[1
,2
]}

Sun, Xuling ^{[1
]}

Luo, Xuelai ^{[1
]}

Wang, Jing ^{[3
]}

Hu, Junbo ^{[1
]}

Feng, Yongdong ^{[1
]}

机构：

[1] Huazhong Univ Sci & Technol, Tongji Med Coll, Tongji Hosp, Dept GI,Canc Res Inst, Wuhan, Hubei, Peoples R China

[2] Huazhong Univ Sci & Technol, Tongji Med Coll, Union Hosp, Dept Breast & Thyroid Surg, Wuhan, Hubei, Peoples R China

[3] Huazhong Univ Sci & Technol, Tongji Med Coll, Dept Immunol, Basic Med, Wuhan, Hubei, Peoples R China

来源：

CELL DEATH & DISEASE | 2020年 / 11卷 / 09期

基金：

中国国家自然科学基金;

关键词：

TUMOR-SUPPRESSOR; UP-REGULATION; CANCER; P21; RB;

D O I：

10.1038/s41419-020-02921-z

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Cellular senescence is a stress response of human cells that removes potentially harmful cells by initiating cell cycle arrest. Inducing senescence of tumor cells may be an effective tumor-inhibiting strategy. In this study we found that PIK3R3 could inhibit the cell senescence of colorectal cancer cells and promote cell proliferation through the p53/p21 signal pathway. PIK3R3 could bind to p53 and inhibit the binding of p53 to the p21 gene promoter region, and thus affecting the transcriptional activity of p21 gene. Our study has provided new evidence of the role of PIK3R3 in p53 regulation and inhibition of PIK3R3 may be one of the potential targets of tumor therapy.

引用

页数：12

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