[Primary research on arsenic trioxide inhibiting human breast cancer cells growth and its mechanisms]

Zhonghua Yi Xue Za Zhi. 2005 May 11;85(17):1209-13.
[Article in Chinese]

Abstract

Objective: The study was to research the biological effect and mechanisms of arsenic trioxide (As2O3) on human breast cancer cell line MDA-MB-231.

Methods: The cytotoxicity was observed by MTT assay. Apoptosis was detected with Annexin V-FITC + PI dual parameter. Cell cycle and positive rate of proliferation cell nuclear antigen (PCNA), apoptosis associated protein Fas and bcl-2 and intracellular calcium ions (IECa(2+)) levels were measured by flow cytometry.

Results: As2O3 could inhibit the growth of MDA-MB-231 cells dramatically. There was obvious dosage-effect correlation (r = 0.99, P < 0.01), its half inhibitory concentration (IC(50)) was 6.65 micromol/L. Apoptosis was observed in MDA-MB-231 cells treated with As2O3. As2O3 could increase Fas expression and IECa(2+) levels and decrease PCNA expression in MDA-MB-231 cells (P < 0.01). Cell cycle was arrested in S + G(2)/M phase, but bcl-2 protein expression were not affected (P > 0.05).

Conclusion: As2O3 could inhibit the growth of MDA-MB-231 cells dramatically and induce apoptosis. We proposed that its mechanisms were probably associated with the improved Fas expression and IECa(2+) levels and decreased PCNA expression and cell cycle arrest.

MeSH terms

  • Antineoplastic Agents / pharmacology*
  • Apoptosis / drug effects*
  • Arsenic Trioxide
  • Arsenicals / pharmacology*
  • Breast Neoplasms / pathology*
  • Calcium / metabolism
  • Cell Division / drug effects*
  • Cell Line, Tumor
  • Female
  • Humans
  • Oxides / pharmacology*
  • Proliferating Cell Nuclear Antigen / biosynthesis
  • fas Receptor / biosynthesis

Substances

  • Antineoplastic Agents
  • Arsenicals
  • Oxides
  • Proliferating Cell Nuclear Antigen
  • fas Receptor
  • Arsenic Trioxide
  • Calcium