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Effects of siRNA-Mediated Knockdown of HDAC1 on the Biological Behavior of Esophageal Carcinoma Cell Lines

BACKGROUND: HDAC1 has been shown to be closely associated with the occurrence of tumors. We aimed to investigate the effects of siRNA-mediated HDAC1 knockdown on the biological behavior of esophageal carcinoma cell lines. MATERIAL/METHODS: HDAC1 expression in esophageal cancer cell lines TE-1, Eca10...

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Autores principales: Wang, Xing, Guo, Haisheng, Liu, Weixin, Yang, Chunmei, Yang, Lei, Wang, Dongguan, Wang, Xunguo
Formato: Online Artículo Texto
Lenguaje:English
Publicado: International Scientific Literature, Inc. 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4837926/
https://www.ncbi.nlm.nih.gov/pubmed/27086779
http://dx.doi.org/10.12659/MSM.895853
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author Wang, Xing
Guo, Haisheng
Liu, Weixin
Yang, Chunmei
Yang, Lei
Wang, Dongguan
Wang, Xunguo
author_facet Wang, Xing
Guo, Haisheng
Liu, Weixin
Yang, Chunmei
Yang, Lei
Wang, Dongguan
Wang, Xunguo
author_sort Wang, Xing
collection PubMed
description BACKGROUND: HDAC1 has been shown to be closely associated with the occurrence of tumors. We aimed to investigate the effects of siRNA-mediated HDAC1 knockdown on the biological behavior of esophageal carcinoma cell lines. MATERIAL/METHODS: HDAC1 expression in esophageal cancer cell lines TE-1, Eca109, and EC9706 was compared by Western blot analysis. These cells were transfected with siRNA-HDAC1 and cell proliferation was evaluated by MTT assay to select the optimum cell line for subsequent experiments. The effects of siRNA-HDAC1 on the migration and invasion of the selected cell line were assessed by transwell assay. The expression of cell cycle-related proteins cyclinD1, p21 and p27, and epithelial-mesenchymal transition (EMT)-related protein zonula occludens-1 (ZO-1), E-cadherin and vimentin was determined by Western blot analysis. RESULTS: HDAC1 expression in TE-1, Eca109 and EC9706 cells was significantly higher compared with normal esophageal cell line HEEC (P<0.01). MTT assay, Western blot and RT-PCR analyses demonstrated that the inhibitory effects of siRNA on HDAC1 expression and cell viability in TE-1 cells were the highest among all cell lines, which was therefore used in subsequent experiments. After TE-1 cells were transfected with siRNA-HDAC1, their migration and invasion were significantly lower compared with the controls (P<0.01). CyclinD1 and vimentin expression was significantly lower compared with the controls (P<0.01), whereas the expression of p21, p27, ZO-1 and E-cadherin was significantly higher (P<0.01). CONCLUSIONS: The siRNA-mediated HDAC1 knockdown significantly inhibited the proliferation, migration and invasion of TE-1 cells probably by regulating the expression of cell cycle- and EMT-related proteins.
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spelling pubmed-48379262016-05-02 Effects of siRNA-Mediated Knockdown of HDAC1 on the Biological Behavior of Esophageal Carcinoma Cell Lines Wang, Xing Guo, Haisheng Liu, Weixin Yang, Chunmei Yang, Lei Wang, Dongguan Wang, Xunguo Med Sci Monit Molecular Biology BACKGROUND: HDAC1 has been shown to be closely associated with the occurrence of tumors. We aimed to investigate the effects of siRNA-mediated HDAC1 knockdown on the biological behavior of esophageal carcinoma cell lines. MATERIAL/METHODS: HDAC1 expression in esophageal cancer cell lines TE-1, Eca109, and EC9706 was compared by Western blot analysis. These cells were transfected with siRNA-HDAC1 and cell proliferation was evaluated by MTT assay to select the optimum cell line for subsequent experiments. The effects of siRNA-HDAC1 on the migration and invasion of the selected cell line were assessed by transwell assay. The expression of cell cycle-related proteins cyclinD1, p21 and p27, and epithelial-mesenchymal transition (EMT)-related protein zonula occludens-1 (ZO-1), E-cadherin and vimentin was determined by Western blot analysis. RESULTS: HDAC1 expression in TE-1, Eca109 and EC9706 cells was significantly higher compared with normal esophageal cell line HEEC (P<0.01). MTT assay, Western blot and RT-PCR analyses demonstrated that the inhibitory effects of siRNA on HDAC1 expression and cell viability in TE-1 cells were the highest among all cell lines, which was therefore used in subsequent experiments. After TE-1 cells were transfected with siRNA-HDAC1, their migration and invasion were significantly lower compared with the controls (P<0.01). CyclinD1 and vimentin expression was significantly lower compared with the controls (P<0.01), whereas the expression of p21, p27, ZO-1 and E-cadherin was significantly higher (P<0.01). CONCLUSIONS: The siRNA-mediated HDAC1 knockdown significantly inhibited the proliferation, migration and invasion of TE-1 cells probably by regulating the expression of cell cycle- and EMT-related proteins. International Scientific Literature, Inc. 2016-04-18 /pmc/articles/PMC4837926/ /pubmed/27086779 http://dx.doi.org/10.12659/MSM.895853 Text en © Med Sci Monit, 2016 This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivs 3.0 Unported License
spellingShingle Molecular Biology
Wang, Xing
Guo, Haisheng
Liu, Weixin
Yang, Chunmei
Yang, Lei
Wang, Dongguan
Wang, Xunguo
Effects of siRNA-Mediated Knockdown of HDAC1 on the Biological Behavior of Esophageal Carcinoma Cell Lines
title Effects of siRNA-Mediated Knockdown of HDAC1 on the Biological Behavior of Esophageal Carcinoma Cell Lines
title_full Effects of siRNA-Mediated Knockdown of HDAC1 on the Biological Behavior of Esophageal Carcinoma Cell Lines
title_fullStr Effects of siRNA-Mediated Knockdown of HDAC1 on the Biological Behavior of Esophageal Carcinoma Cell Lines
title_full_unstemmed Effects of siRNA-Mediated Knockdown of HDAC1 on the Biological Behavior of Esophageal Carcinoma Cell Lines
title_short Effects of siRNA-Mediated Knockdown of HDAC1 on the Biological Behavior of Esophageal Carcinoma Cell Lines
title_sort effects of sirna-mediated knockdown of hdac1 on the biological behavior of esophageal carcinoma cell lines
topic Molecular Biology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4837926/
https://www.ncbi.nlm.nih.gov/pubmed/27086779
http://dx.doi.org/10.12659/MSM.895853
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