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Updated: Feb 12, 2026

Techniques to Induce and Quantify Cellular Senescence
06:51

Techniques to Induce and Quantify Cellular Senescence

Published on: May 1, 2017

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Down-regulation of cancer-associated gene CDC73 contributes to cellular senescence

Qi Jia1, Hongbo Nie1, Xuechao Wan2

  • 1Ministry of Education Key Laboratory of Contemporary Anthropology, Collaborative Innovation Center of Genetics and Development, School of Life Sciences and Huashan Hospital, Fudan University, Shanghai, 200438, China.

Biochemical and Biophysical Research Communications
|April 6, 2018
PubMed

Insights

Cell division cycle 73 (CDC73) is down-regulated in senescent cells, promoting cancer prevention. This post-transcriptional regulation, via alternative polyadenylation, offers potential anti-cancer therapy strategies.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Cellular Biology

Background:

  • Gene expression dysregulation contributes to cancer phenotypes beyond mutations.
  • Cellular senescence is a crucial tumor-preventive mechanism.
  • Understanding gene expression regulation in senescence is key for anti-cancer therapies.

Purpose of the Study:

  • Investigate the role of CDC73 in cellular senescence and cancer.
  • Elucidate the molecular mechanisms behind CDC73 dysregulation in senescence.
  • Explore the therapeutic potential of targeting CDC73 in cancer.

Main Methods:

  • Analysis of CDC73 expression in cancer types and senescent cells.
  • Depletion of CDC73 in normal and cancer cells to assess senescence induction.
  • Investigation of alternative polyadenylation (APA) and 3' UTR length in CDC73 regulation.

Main Results:

  • CDC73 was unexpectedly up-regulated in cancers but down-regulated in senescent cells.
  • CDC73 depletion induced senescence-associated phenotypes and increased p21 expression.
  • APA-mediated 3' UTR lengthening contributed to decreased CDC73 expression in senescent cells.

Conclusions:

  • Post-transcriptional down-regulation of CDC73 is a significant factor in cellular senescence.
  • CDC73's role in senescence suggests its potential as a therapeutic target for cancer.
  • Alternative polyadenylation is a key mechanism controlling CDC73 expression during senescence.
Keywords:
3′ UTRCDC73CancerCellular senescenceGene expression

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