2008•Zhonghua zhongliu fangzhi zazhiRequires access

Effect of As4S4 on preliferation, apoptosis and COX-2 expression of human cervical carcinoma HeLa cells

Li Tian

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Abstract

OBJECTIVE:To investigate the HeLa cell growth inhibition and apoptosis induced by As4S4 and the relationship with COX-2 expression in vitro. METHODS: HeLa cells were treated with various concentrations (7.5-60 mg/L) of As4S4 for 12-60 h.The cell growth rate was measured by MTT; apoptosis was detected by DNA electrophoresis.The levels of PGE2 were measured by radioimmunoassay. The expression of COX-2 protein was also examined by Western blot analysis. RESULTS: After treated with different concentrations of As4S4, the cell growth of HeLa was suppressed significantly in dose and time-dependent manner in proliferative inhibition rate, P0.01. As4S4 induced the apoptosis and DNA fragmentation gel analysis showed DNA ladder. As4S4 reduced the release of PGE2 in HeLa cells with the values being (70.56±2.03),(48.58±2.28),(29.25±1.57) and (18.02±1.04) μg/L, respectively, as compared with control group (83.15±0.01) μg/L, P0.01. As4S4 inhibited the activity and expression of COX-2 with the rise of concentration, and it down-regulated the expression of COX-2 protein significantly. CONCLUSIONS: As4S4 can inhibit the proliferation and increase apoptosis in human HeLa cells. These effects may depend on the inhibition of the expression of COX-2 and level of PGE2 by As4S4.

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OBJECTIVE:To investigate the HeLa cell growth inhibition and apoptosis induced by As4S4 and the relationship with COX-2 expression in vitro. METHODS: HeLa cells were treated with various concentrations (7.5-60 mg/L) of As4S4 for 12-60 h.The cell growth rate was measured by MTT; apoptosis was detected by DNA electrophoresis.The levels of PGE2 were measured by radioimmunoassay. The expression of COX-2 protein was also examined by Western blot analysis. RESULTS: After treated with different concentrations of As4S4, the cell growth of HeLa was suppressed significantly in dose and time-dependent manner in proliferative inhibition rate, P0.01. As4S4 induced the apoptosis and DNA fragmentation gel analysis showed DNA ladder. As4S4 reduced the release of PGE2 in HeLa cells with the values being (70.56±2.03),(48.58±2.28),(29.25±1.57) and (18.02±1.04) μg/L, respectively, as compared with control group (83.15±0.01) μg/L, P0.01. As4S4 inhibited the activity and expression of COX-2 with the rise of concentration, and it down-regulated the expression of COX-2 protein significantly. CONCLUSIONS: As4S4 can inhibit the proliferation and increase apoptosis in human HeLa cells. These effects may depend on the inhibition of the expression of COX-2 and level of PGE2 by As4S4.

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Available abstract

OBJECTIVE:To investigate the HeLa cell growth inhibition and apoptosis induced by As4S4 and the relationship with COX-2 expression in vitro. METHODS: HeLa cells were treated with various concentrations (7.5-60 mg/L) of As4S4 for 12-60 h.The cell growth rate was measured by MTT; apoptosis was detected by DNA electrophoresis.The levels of PGE2 were measured by radioimmunoassay. The expression of COX-2 protein was also examined by Western blot analysis. RESULTS: After treated with different concentrations of As4S4, the cell growth of HeLa was suppressed significantly in dose and time-dependent manner in proliferative inhibition rate, P0.01. As4S4 induced the apoptosis and DNA fragmentation gel analysis showed DNA ladder. As4S4 reduced the release of PGE2 in HeLa cells with the values being (70.56±2.03),(48.58±2.28),(29.25±1.57) and (18.02±1.04) μg/L, respectively, as compared with control group (83.15±0.01) μg/L, P0.01. As4S4 inhibited the activity and expression of COX-2 with the rise of concentration, and it down-regulated the expression of COX-2 protein significantly. CONCLUSIONS: As4S4 can inhibit the proliferation and increase apoptosis in human HeLa cells. These effects may depend on the inhibition of the expression of COX-2 and level of PGE2 by As4S4.

Key concepts: HeLa, Apoptosis, Western blot, DNA fragmentation, Molecular biology, Biology, Fragmentation (computing), Growth inhibition

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