Anti-apoptotic and apoptotic pathway analysis of arsenic trioxide‑induced apoptosis in human gastric cancer SGC-7901 cells

Yu,Yao; Yang,Yu; Wang,Jing

doi:10.3892/or.2014.3276

Anti-apoptotic and apoptotic pathway analysis of arsenic trioxide‑induced apoptosis in human gastric cancer SGC-7901 cells

Authors:
- Yao Yu
- Yu Yang
- Jing Wang
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Affiliations: Department of Oncology, The Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150086, P.R. China
Published online on: June 20, 2014 https://doi.org/10.3892/or.2014.3276
Pages: 973-978

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Abstract

The present study aimed to investigate the effect of arsenic trioxide (As2O3) on human gastric cancer SGC-7901 cells. SGC-7901 cells were treated with different concentrations of As2O3 in the cell growth media for 24, 48 and 72 h, and the growth rates were determined by WST-1 cell proliferation assays. Analyses of nuclear morphological changes were performed with DAPI fluorescence staining. Cell apoptosis rates as assessed by flow cytometry were determined after cells were grown in media for 48 h containing different As2O3 concentrations. The protein expression patterns of the apoptosis factors, Bax, Fas and caspase-8, and anti-apoptosis factors, Akt, p-Akt, mTOR and p-mTOR, were evaluated by western blot analysis following treatment of the cells with different As2O3 concentrations in the cell growth media for 48 h. As a result, As2O3 inhibited the growth of human gastric cancer SGC-7901 cells in concentrations >5 µmol/l for longer than 24 h. Flow cytometric analysis revealed that the apoptosis of SGC-7901 cells occurred in an As2O3 concentration-dependent manner after 48 h (P<0.001). Expression levels of Bax, Fas and caspase-8 were increased, whereas expression levels of Akt, p-Akt, mTOR and p-mTOR were decreased in the SGC-7901 cells after a 48-h incubation with different As2O3 concentrations. In conclusion, As2O3 induced human gastric cancer SGC-7901 cell apoptosis in a time- and concentration dependent manner by inhibiting the activity of anti-apoptosis-related factors.

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