1. Academic Validation
  2. PIK3R3 inhibits cell senescence through p53/p21 signaling

PIK3R3 inhibits cell senescence through p53/p21 signaling

  • Cell Death Dis. 2020 Sep 24;11(9):798. doi: 10.1038/s41419-020-02921-z.
Qianzhi Chen 1 2 Xuling Sun 1 Xuelai Luo 1 Jing Wang 3 Junbo Hu 4 Yongdong Feng 5
Affiliations

Affiliations

  • 1 Department of GI Cancer Research Institute, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China.
  • 2 Department of Breast and Thyroid Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China.
  • 3 Department of Immunology, Basic of Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China.
  • 4 Department of GI Cancer Research Institute, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China. jbhu@tjh.tjmu.edu.cn.
  • 5 Department of GI Cancer Research Institute, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China. ydfeng@tjh.tjmu.edu.cn.
Abstract

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.

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