2013•TumoriRequires access

Effects of all-trans retinoic acid on proliferation, cell cycle and apoptosis of human esophageal squamous cancer EC1 cells

Yihao Yao, Yanxia Ding, Jindong Zhang, Xiaona Wang, Xiaolong Wu, Youtian Huang, Hongyan Yang, Jimin Zhao, Ziming Dong

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Abstract

Objective: To investigate the effects of ATRA (all-trans retinoic acid) on cell proliferation, cell cycle and apoptosis of human esophageal squamous cancer EC1 cells, and to explore its possible mechanism. Methods: The abilities of cellular proliferation of EC1 cells after treatment with 1, 10 and 20 μmol/L ATRA were detected by MTT assay, and the cell cycle distribution and the apoptosis of EC1 cells were determined by flow cytometry. The expressions of p21 and Bcl-2 in EC1 cells after treatment with 1, 10 and 20 μmol/L ATRA were detected by immunocytochemistry and Western blotting. Results: As compared with the EC1 cells without treatment (as a control), the proliferation of EC1 cells was inhibited by ATRA in a dose- and time-dependent manner (P < 0.05). The proportions of G0 and G1 cells were higher in EC1 cells after treatment with 1, 10 and 20 μmol/L ATRA than that of the control cells [(66.58±0.30)%, (67.96±0.77)% and (75.11±2.24)% vs (59.90±0.82)%, P < 0.05]. The apoptotic rates of EC1 cells treated with 1, 10 and 20 μmol/L ATRA were higher than that of the control cells [(4.86±0.04)%, (7.35±0.04)% and (12.03±0.12)% vs (3.17±0.05)%, P < 0.05]. The expression level of p21 in EC1 cells treated with ATRA was up-regulated, but the expression level of Bcl-2 was down-regulated. Conclusion: ATRA can inhibit the proliferation of human esophageal squamous cancer EC1 cells and induce G0/G1 phase blocking and cell apoptosis. This effect may be related with the up-regulation of p21 expression and down-regulation of Bcl-2 expression. DOI:10.3781/j.issn.1000-7431.2013.08.005

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What this paper is about

Objective: To investigate the effects of ATRA (all-trans retinoic acid) on cell proliferation, cell cycle and apoptosis of human esophageal squamous cancer EC1 cells, and to explore its possible mechanism. Methods: The abilities of cellular proliferation of EC1 cells after treatment with 1, 10 and 20 μmol/L ATRA were detected by MTT assay, and the cell cycle distribution and the apoptosis of EC1 cells were determined by flow cytometry. The expressions of p21 and Bcl-2 in EC1 cells after treatment with 1, 10 and 20 μmol/L ATRA were detected by immunocytochemistry and Western blotting. Results: As compared with the EC1 cells without treatment (as a control), the proliferation of EC1 cells was inhibited by ATRA in a dose- and time-dependent manner (P < 0.05). The proportions of G0 and G1 cells were higher in EC1 cells after treatment with 1, 10 and 20 μmol/L ATRA than that of the control cells [(66.58±0.30)%, (67.96±0.77)% and (75.11±2.24)% vs (59.90±0.82)%, P < 0.05]. The apoptotic rates of EC1 cells treated with 1, 10 and 20 μmol/L ATRA were higher than that of the control cells [(4.86±0.04)%, (7.35±0.04)% and (12.03±0.12)% vs (3.17±0.05)%, P < 0.05]. The expression level of p21 in EC1 cells treated with ATRA was up-regulated, but the expression level of Bcl-2 was down-regulated. Conclusion: ATRA can inhibit the proliferation of human esophageal squamous cancer EC1 cells and induce G0/G1 phase blocking and cell apoptosis. This effect may be related with the up-regulation of p21 expression and down-regulation of Bcl-2 expression. DOI:10.3781/j.issn.1000-7431.2013.08.005

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Available abstract

Objective: To investigate the effects of ATRA (all-trans retinoic acid) on cell proliferation, cell cycle and apoptosis of human esophageal squamous cancer EC1 cells, and to explore its possible mechanism. Methods: The abilities of cellular proliferation of EC1 cells after treatment with 1, 10 and 20 μmol/L ATRA were detected by MTT assay, and the cell cycle distribution and the apoptosis of EC1 cells were determined by flow cytometry. The expressions of p21 and Bcl-2 in EC1 cells after treatment with 1, 10 and 20 μmol/L ATRA were detected by immunocytochemistry and Western blotting. Results: As compared with the EC1 cells without treatment (as a control), the proliferation of EC1 cells was inhibited by ATRA in a dose- and time-dependent manner (P < 0.05). The proportions of G0 and G1 cells were higher in EC1 cells after treatment with 1, 10 and 20 μmol/L ATRA than that of the control cells [(66.58±0.30)%, (67.96±0.77)% and (75.11±2.24)% vs (59.90±0.82)%, P < 0.05]. The apoptotic rates of EC1 cells treated with 1, 10 and 20 μmol/L ATRA were higher than that of the control cells [(4.86±0.04)%, (7.35±0.04)% and (12.03±0.12)% vs (3.17±0.05)%, P < 0.05]. The expression level of p21 in EC1 cells treated with ATRA was up-regulated, but the expression level of Bcl-2 was down-regulated. Conclusion: ATRA can inhibit the proliferation of human esophageal squamous cancer EC1 cells and induce G0/G1 phase blocking and cell apoptosis. This effect may be related with the up-regulation of p21 expression and down-regulation of Bcl-2 expression. DOI:10.3781/j.issn.1000-7431.2013.08.005

Key concepts: Apoptosis, Cell cycle, Cell growth, Retinoic acid, Flow cytometry, MTT assay, Cell, Chemistry

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Effects of all-trans retinoic acid on proliferation, cell cycle and apoptosis of human esophageal squamous cancer EC1 cells — Research Paper | ScholarLens