[Arsenic trioxide induced apoptosis in retinoblastoma cells in vitro and its possible mechanism]

Zhong Nan Da Xue Xue Bao Yi Xue Ban. 2008 Jun;33(6):476-80.
[Article in Chinese]

Abstract

Objective: To explore the effect of arsenic trioxide on the apoptosis of retinoblastoma cell line HXO-RB(44) and the possible mechanism.

Methods: The effect of arsenic trioxide on the proliferation of retinoblastoma cell line HXO-RB(44) was observed by MTT colorimetric assay; the apoptosis of the HXO-RB(44) was examined by AO/EB staining and flow cytometry analysis (Annexin V+ PI staining); caspase-3 activity and bcl-2/bax expression in the HXO-RB(44) were detected by cpp32 colorimetric assay kit and Western blot.

Results: Arsenic trioxide inhibited the proliferation of HXO-RB(44) cell in dose and duration-dependent manner in vitro; arsenic trioxide significantly increased the apoptosis in HXO-RB(44) cells. The activation of caspase-3 was increased, and the rate of bcl-2/bax was down-regulated in the HXO-RB(44) cells processed with arsenic trioxide.

Conclusion: Arsenic trioxide can inhibit the proliferation of retinoblastoma cell HXO-RB(44) in vitro by apoptosis induction. The apoptosis induction is possibly related to the caspase-3 activation and bcl-2/bax down-regulation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antineoplastic Agents / pharmacology
  • Apoptosis / drug effects*
  • Arsenic Trioxide
  • Arsenicals / pharmacology*
  • Caspase 3 / biosynthesis
  • Humans
  • Oxides / pharmacology*
  • Proto-Oncogene Proteins c-bcl-2 / biosynthesis
  • Retinal Neoplasms / pathology*
  • Retinoblastoma / pathology*
  • Tumor Cells, Cultured
  • bcl-2-Associated X Protein / biosynthesis

Substances

  • Antineoplastic Agents
  • Arsenicals
  • Oxides
  • Proto-Oncogene Proteins c-bcl-2
  • bcl-2-Associated X Protein
  • Caspase 3
  • Arsenic Trioxide