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Yeast As a Chassis for Developing Functional Assays to Study Human P53
14:57

Yeast As a Chassis for Developing Functional Assays to Study Human P53

Published on: August 4, 2019

Exit from arsenite-induced mitotic arrest is p53 dependent

Samuel C McNeely1, Xiaogiang Xu, B Frazier Taylor

  • 1Department of Pharmacology and Toxicology, University of Louisville, Louisville, Kentucky, USA.

Environmental Health Perspectives
|September 13, 2006
PubMed
Abstract

Insights

The tumor suppressor p53 helps cells exit mitosis after arsenite exposure. This process involves increased induction of inhibitor of DNA binding-1 (ID1), potentially impacting arsenic carcinogenicity.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Cell Biology

Background:

  • Arsenic is a known human carcinogen and a chemotherapeutic agent, but its mechanisms remain unclear.
  • The role of p53 in arsenic's effects on cell division and death is not well understood.
  • Previous studies showed arsenite disrupts mitosis and that p53-deficient cells are more sensitive to its effects.

Purpose of the Study:

  • To investigate the protective role of p53 against arsenite-induced mitotic arrest.
  • To understand how p53 influences cell cycle progression following arsenite exposure.

Main Methods:

  • Synchronized p53-expressing (p53(+)) and p53-deficient (p53(-)) cells were treated with sodium arsenite.
  • Mitotic index analysis was used to assess cell cycle progression.
  • Microarray and immunoblotting were employed to analyze gene expression, specifically inhibitor of DNA binding-1 (ID1).

Main Results:

  • Arsenite delayed G2 phase exit in both p53(+) and p53(-) cells.
  • p53(+) cells exited mitosis more efficiently than p53(-) cells.
  • Arsenite induced ID1 expression more extensively and persistently in p53(+) cells compared to p53(-) cells.

Conclusions:

  • p53 facilitates mitotic exit in cells exposed to arsenite.
  • p53 enhances arsenite-induced ID1 expression.
  • ID1 may contribute to cell survival in arsenite-treated cells and play a role in arsenic-induced carcinogenesis.

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