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Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
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Cell Death Associated with Abnormal Mitosis Observed by Confocal Imaging in Live Cancer Cells
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miR-34a is essential for p19(Arf)-driven cell cycle arrest.

Nida Iqbal1, Jie Mei2, Jing Liu1

  • 1Division of Hematology/Oncology; Department of Pediatrics; University of Texas Southwestern Medical Center; Dallas, TX USA.

Cell Cycle (Georgetown, Tex.)
|January 10, 2014
PubMed
Summary

The Arf tumor suppressor regulates cell proliferation independently of p53 by controlling miR-34a. This microRNA targets Pdgfrβ, impacting vision and development.

Keywords:
Pdgfrβcell cyclemiR-34ap19Arfp53tumor suppressionvascular remodeling

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Area of Science:

  • Molecular Biology
  • Genetics
  • Developmental Biology

Background:

  • The Arf tumor suppressor (p19Arf) regulates cell proliferation in cancer and development.
  • p19Arf exerts functions both dependent and independent of p53.
  • p53-independent repression of Platelet-Derived Growth Factor Receptor beta (Pdgfrβ) by p19Arf is crucial for vision.

Purpose of the Study:

  • To define the role of microRNA-34a (miR-34a) in the p53-independent repression of Pdgfrβ by p19Arf.
  • To investigate the mechanism linking p19Arf, miR-34a, and Pdgfrβ in cell proliferation control.

Main Methods:

  • Cell culture experiments with ectopic Arf expression and anti-miR-34a treatment.
  • Mouse embryo fibroblast (MEF) models lacking p53.
  • Reporter assays to confirm direct targeting of Pdgfrβ by miR-34a.
  • In vivo analysis of Arf and miR-34 family expression in mouse embryonic eyes.

Main Results:

  • Ectopic Arf expression increased miR-34 family microRNAs targeting Pdgfrβ.
  • In p53-deficient MEFs, Arf-mediated repression of Pdgfrβ and Pdgf-B-induced DNA synthesis was dependent on miR-34a.
  • miR-34a directly targeted Pdgfrβ, confirmed by reporter assays.
  • Arf controlled miR-34a, miR-34b, and miR-34c expression in vivo during mouse development.

Conclusions:

  • miR-34a acts as a critical mediator of p19Arf's p53-independent tumor suppressor function.
  • The p19Arf-miR-34a-Pdgfrβ axis is essential for regulating cell proliferation and has implications for vision and cancer development.
  • This study reveals a novel mechanism for Arf's tumor suppressor activity during development and in incipient cancer cells.