Arsenic compounds induce apoptosis through caspase pathway activation in MA-10 leydig tumor cells

Yi Fen Mu, Ying Hui Chen, Ming Min Chang, Yung Chia Chen, Bu Miin Huang

Research output: Contribution to journalArticle

1 Citation (Scopus)

Abstract

The incidence of testicular cancer is increasing worldwide. Leydig cell tumors represent one type of sex cord-stromal testis malignancy, which tend to respond unfavorably to chemotherapies. Identifying more efficient treatment strategies is therefore crucial for patients. The present study aimed to investigate the apoptotic effects of arsenic compounds and their underlying mechanisms. The results indicated that sodium arsenite and dimethylarsenic acid induced apoptosis of the murine Leydig tumor cell line, MA-10. These apoptotic effects were characterized morpho-logically by membrane blebbing and cell detachment assays, biochemically using a cell viability assay, and cytologically by flow cytometry analysis. Western blotting demonstrated that caspases-3, -8 and -9, and poly(ADP-ribose) polymerase protein levels were increased compared with untreated MA-10 cells; however, the caspase inhibitor, Z-VAD-fmk, reversed these effects. In conclusion, the present study has shown that sodium arsenite and dimethylarsenic acid may activate the intrinsic and extrinsic caspase pathways, and induce MA-10 cell apoptosis. These results suggest that sodium arsenite and dimethylarsenic acid may represent novel approaches to treat clinically unmanageable forms of testicular cancer.

Original languageEnglish
Pages (from-to)944-954
Number of pages11
JournalOncology Letters
Volume18
Issue number1
DOIs
Publication statusPublished - 2019 Jan 1

All Science Journal Classification (ASJC) codes

  • Oncology
  • Cancer Research

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