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2018•Zhonghua shiyan waike zazhiRequires access

Sodium selenite combined prodrug of adriamycin mediated the proliferation and apoptosis of gastric cancer cell SGC-7901 through mitogen-activated protein kinase signal pathway

Quanfeng Wu, Xiaojun Fang, Xiaoqin Yang, Yuanxing Chen, Bitao Zhang, Juan Zhang, Jianhua Sun

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Abstract

Objective To investigate the effects of sodium selenite combined with prodrug of adriamycin (PADM) on the proliferation and apoptosis of gastric cancer cell SGC-7901. Methods According to half maximal inhibitory concentration (IC50) from the pre-experiment, the SGC-7901 cells were treated with 2.93 μg/ml sodium selenite and 2 μg/ml PADM. After treatment with 48 h, methyl thiazol tetrazolium (MTT) assay was used to detect the proliferation of SGC-7901 cells. The apoptosis of SGC-7901 cells was detected by flow cytometry. The expression of mitogen-activated protein kinase (MAPK) signal related mRNAs were measured using reverse transcriptase-polymerase chain reaction (RT-PCR) and the activation of MAPK signal was detected using Western blotting. Results Compared with control (0.873±0.055), Sodium selenite (0.551±0.032) and PADM (0.610±0.023) can significantly reduce the proliferation of gastric cancer SGC-7901 cells (P=0.001, 0.001). The proliferation of SGC-7901 cells was inhibited in Sodium selenite combined with PADM (0.234±0.022) compared with single (P=0.000, 0.000). Compared with control (11.413±1.676), Sodium selenite (23.530±0.943) and PADM (23.207±2.294) can markedly promote the apoptosis of SGC-7901 cells (P=0.000, 0.001). The apoptosis of SGC-7901 cells was increased in Sodium selenite combined with PADM (54.827±4.048) compared with single (P=0.000, 0.000). Sodium selenite and PADM significantly decreased the mRNA expression and activation of extracellular signal-regulated kinase 1/2 (ERK1/2), up-regulated mRNA expression and activation of p38MAPK and c-Jun N-terminal kinase (JNK). The effect was more pronounced after the combination of the two drugs. Conclusion Sodium selenite joint PADM can obviously inhibit proliferation of gastric cancer SGC-7901 cells, promote apoptosis of the SGC-7901 cell. Its mechanism may be related to inhibition of ERK1/2 activation, promotion of p38MAPK and JNK activation. Key words: Sodium selenite; Prodrug of adriamycin; Gastric cancer cells SGC-7901; Mitogen-activated protein kinase signal pathway

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Objective To investigate the effects of sodium selenite combined with prodrug of adriamycin (PADM) on the proliferation and apoptosis of gastric cancer cell SGC-7901. Methods According to half maximal inhibitory concentration (IC50) from the pre-experiment, the SGC-7901 cells were treated with 2.93 μg/ml sodium selenite and 2 μg/ml PADM. After treatment with 48 h, methyl thiazol tetrazolium (MTT) assay was used to detect the proliferation of SGC-7901 cells. The apoptosis of SGC-7901 cells was detected by flow cytometry. The expression of mitogen-activated protein kinase (MAPK) signal related mRNAs were measured using reverse transcriptase-polymerase chain reaction (RT-PCR) and the activation of MAPK signal was detected using Western blotting. Results Compared with control (0.873±0.055), Sodium selenite (0.551±0.032) and PADM (0.610±0.023) can significantly reduce the proliferation of gastric cancer SGC-7901 cells (P=0.001, 0.001). The proliferation of SGC-7901 cells was inhibited in Sodium selenite combined with PADM (0.234±0.022) compared with single (P=0.000, 0.000). Compared with control (11.413±1.676), Sodium selenite (23.530±0.943) and PADM (23.207±2.294) can markedly promote the apoptosis of SGC-7901 cells (P=0.000, 0.001). The apoptosis of SGC-7901 cells was increased in Sodium selenite combined with PADM (54.827±4.048) compared with single (P=0.000, 0.000). Sodium selenite and PADM significantly decreased the mRNA expression and activation of extracellular signal-regulated kinase 1/2 (ERK1/2), up-regulated mRNA expression and activation of p38MAPK and c-Jun N-terminal kinase (JNK). The effect was more pronounced after the combination of the two drugs. Conclusion Sodium selenite joint PADM can obviously inhibit proliferation of gastric cancer SGC-7901 cells, promote apoptosis of the SGC-7901 cell. Its mechanism may be related to inhibition of ERK1/2 activation, promotion of p38MAPK and JNK activation. Key words: Sodium selenite; Prodrug of adriamycin; Gastric cancer cells SGC-7901; Mitogen-activated protein kinase signal pathway

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Available abstract

Objective To investigate the effects of sodium selenite combined with prodrug of adriamycin (PADM) on the proliferation and apoptosis of gastric cancer cell SGC-7901. Methods According to half maximal inhibitory concentration (IC50) from the pre-experiment, the SGC-7901 cells were treated with 2.93 μg/ml sodium selenite and 2 μg/ml PADM. After treatment with 48 h, methyl thiazol tetrazolium (MTT) assay was used to detect the proliferation of SGC-7901 cells. The apoptosis of SGC-7901 cells was detected by flow cytometry. The expression of mitogen-activated protein kinase (MAPK) signal related mRNAs were measured using reverse transcriptase-polymerase chain reaction (RT-PCR) and the activation of MAPK signal was detected using Western blotting. Results Compared with control (0.873±0.055), Sodium selenite (0.551±0.032) and PADM (0.610±0.023) can significantly reduce the proliferation of gastric cancer SGC-7901 cells (P=0.001, 0.001). The proliferation of SGC-7901 cells was inhibited in Sodium selenite combined with PADM (0.234±0.022) compared with single (P=0.000, 0.000). Compared with control (11.413±1.676), Sodium selenite (23.530±0.943) and PADM (23.207±2.294) can markedly promote the apoptosis of SGC-7901 cells (P=0.000, 0.001). The apoptosis of SGC-7901 cells was increased in Sodium selenite combined with PADM (54.827±4.048) compared with single (P=0.000, 0.000). Sodium selenite and PADM significantly decreased the mRNA expression and activation of extracellular signal-regulated kinase 1/2 (ERK1/2), up-regulated mRNA expression and activation of p38MAPK and c-Jun N-terminal kinase (JNK). The effect was more pronounced after the combination of the two drugs. Conclusion Sodium selenite joint PADM can obviously inhibit proliferation of gastric cancer SGC-7901 cells, promote apoptosis of the SGC-7901 cell. Its mechanism may be related to inhibition of ERK1/2 activation, promotion of p38MAPK and JNK activation. Key words: Sodium selenite; Prodrug of adriamycin; Gastric cancer cells SGC-7901; Mitogen-activated protein kinase signal pathway

Key concepts: Apoptosis, MAPK/ERK pathway, Chemistry, Molecular biology, Cell growth, Kinase, Cancer cell, MTT assay

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Sodium selenite combined prodrug of adriamycin mediated the proliferation and apoptosis of gastric cancer cell SGC-7901 through mitogen-activated protein kinase signal pathway — Research Paper | ScholarLens