Overexpression of splicing factor poly(rC)-binding protein 1 elicits cycle arrest, apoptosis induction, and p73

Yuhong Chen1,2,3,4, Zhihui Dou1,2,3,4, Xiaohua Chen1,2,3,4

  • 1Bio-Medical Research Center, Institute of Modern Physics, Chinese Academy of Sciences, Lanzhou, 730000, China.

Abstract

Insights

Splicing factor PCBP1 suppresses cervical cancer growth by inducing apoptosis and cell cycle arrest. Targeting PCBP1 may offer a new therapeutic strategy for cervical cancer.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Cell Biology

Background:

  • Splicing factor poly(rC)-binding protein 1 (PCBP1) is a tumor suppressor implicated in cancer progression.
  • The specific role of PCBP1 in cancer cell apoptosis and its underlying mechanisms are not fully understood.

Purpose of the Study:

  • To investigate the function of PCBP1 in apoptosis of human cervical cancer cells.
  • To elucidate the molecular mechanisms by which PCBP1 influences cancer cell fate.

Main Methods:

  • Overexpression of PCBP1 in human cervical cancer cells (HeLa).
  • Assessment of cell proliferation, cell cycle progression, and apoptosis using cytological assays.

Main Results:

  • PCBP1 overexpression significantly inhibited HeLa cell proliferation in a time-dependent manner.
  • PCBP1 induced G2/M phase arrest and increased apoptosis.
  • PCBP1 promoted the production of long p73 isoforms, leading to an altered Bax/Bcl-2 ratio, cytochrome c release, and caspase-3 activation.

Conclusions:

  • PCBP1 plays a critical role in regulating p73 splicing, cell cycle arrest, and apoptosis in cervical cancer cells.
  • PCBP1 represents a potential therapeutic target for cervical cancer treatment.

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