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Different pathways are involved in arsenic-trioxide-induced cell proliferation and growth inhibition in human

X Bi1, J Gu, Z Guo

  • 1Department of Dermatology, Changhai Hospital, Second Military Medical University, Shanghai, PR China.

Skin Pharmacology and Physiology
|December 18, 2009
PubMed
Abstract

Insights

Arsenic trioxide (As(2)O(3)) shows dual effects: low doses promote keratinocyte proliferation, while high doses induce apoptosis and cell cycle arrest. Skin carcinoma cells, however, are resistant to As(2)O(3) growth inhibition.

Area of Science:

  • Toxicology
  • Molecular Biology
  • Dermatology

Background:

  • Arsenic is a known carcinogen linked to skin cancer.
  • Arsenic trioxide (As(2)O(3)) exhibits potential anticancer properties.
  • The mechanisms behind arsenic's opposing effects on skin cells are not fully understood.

Purpose of the Study:

  • To investigate the effects of As(2)O(3) on keratinocyte proliferation and growth inhibition.
  • To explore the molecular pathways influenced by As(2)O(3) in normal and cancerous skin cells.

Main Methods:

  • Utilized normal human keratinocytes (NHK), HaCaT cells, and A431 epidermal carcinoma cells.
  • Exposed cells to varying concentrations of As(2)O(3) (0.5-32 nM and 0.5-10 microM).
  • Assessed cell proliferation, gene expression, apoptosis (caspase-3 activation), and cell cycle progression (G2-M arrest).

Main Results:

  • Low As(2)O(3) concentrations (0.5-32 nM) enhanced keratinocyte proliferation and upregulated cell cycling genes (e.g., CDK4, E2F1).
  • High As(2)O(3) concentrations (0.5-10 microM) inhibited NHK and HaCaT cell growth, induced apoptosis via caspase-3, and caused G2-M cell cycle arrest.
  • A431 skin carcinoma cells demonstrated resistance to As(2)O(3)-induced growth inhibition and apoptosis.

Conclusions:

  • As(2)O(3) exerts differential effects on skin cells, promoting proliferation at low doses and inducing cell death at high doses.
  • Skin carcinoma cells exhibit resistance to the cytotoxic effects of As(2)O(3).
  • As(2)O(3) may not be a suitable therapeutic agent for treating skin carcinomas due to observed resistance.

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