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Updated: Jun 28, 2026

A Quantitative Measurement of Reactive Oxygen Species and Senescence-associated Secretory Phenotype in Normal Human Fibroblasts During Oncogene-induced Senescence
13:59

A Quantitative Measurement of Reactive Oxygen Species and Senescence-associated Secretory Phenotype in Normal Human Fibroblasts During Oncogene-induced Senescence

Published on: August 12, 2018

CARF Is a vital dual regulator of cellular senescence and apoptosis

Kamrul Hasan1, Caroline Cheung, Zeenia Kaul

  • 1National Institute of Advanced Industrial Science & Technology (AIST), 1-1-1 Higashi, Tsukuba, Ibaraki 305-8562, Japan.

The Journal of Biological Chemistry
|November 13, 2008
PubMed

Insights

Collaborator of ARF (CARF) protein overexpression induces premature senescence in human fibroblasts. CARF is essential for senescence and its absence leads to aneuploidy and apoptosis, revealing its dual role in tumor suppression.

Area of Science:

  • Molecular and Cellular Biology
  • Cancer Research
  • Tumor Suppressor Pathways

Background:

  • The p53 protein is a critical tumor suppressor involved in DNA repair, cell cycle control, and aging.
  • Complex regulatory networks govern p53 activity, including upstream sensors, downstream effectors, and feedback loops.
  • Collaborator of ARF (CARF) has been previously identified to enhance wild-type p53 function.

Purpose of the Study:

  • To investigate the role of CARF in regulating cellular senescence and apoptosis.
  • To elucidate the function of CARF in p53-mediated tumor suppressor mechanisms.

Main Methods:

  • Overexpression of CARF in human fibroblasts.
  • Analysis of replicative and stress-induced senescence.
  • Assessment of aneuploidy and apoptosis in CARF-deficient cells.

Main Results:

  • CARF overexpression induced premature senescence in human fibroblasts.
  • CARF was found to be essential for both replicative and stress-induced senescence.
  • Loss of CARF function resulted in aneuploidy and apoptosis.

Conclusions:

  • CARF plays a crucial dual role in p53-mediated senescence and apoptosis.
  • CARF is vital for maintaining genomic stability and preventing tumorigenesis.
  • These findings highlight CARF as a key regulator in major tumor suppressor pathways.

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