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Effect of DAPPER1 on malignant biological behavior of esophageal carcinoma cells and its epigenetic regulatory mechanism / 临床与实验病理学杂志
Chinese Journal of Clinical and Experimental Pathology ; (12): 827-831, 2017.
Article in Chinese | WPRIM | ID: wpr-668057
ABSTRACT
Purpose To investigate the effect of DAPPER1 on the malignant biological behavior in esophageal carcinoma cells,and further to analyze the expression and the possible regulated mechanism of DAPPER1 in esophageal squamous cell cancer (ESCC) samples.Methods MTT assay,colony formation assay and wound healing were used to examine the effect of DAPPER1 on malignant biological behavior in esophageal carcinoma cells,RT-PCR and MSP methods were applied respectively to examine the expression and the methylation status of DAP-PER1 in three ESCC cell lines (TE13,T.Tn,Eca109).Immunohistochemistry was used to examine the DAPPER1 protein expression.Results The negative or weak expression of DAP-PER1 was detected in ESCC cell lines.After treated with 5-Aza2'-deoxycytidine (5-Aza-dC,a demethylation agent),the expression level of DAPPER1 was obviously increased.Meanwhile,over expression of DAPPER1 or treated with 5-Aza-Dc could obviously inhibit proliferation and immigration abilities of TEl3 cell line.The level of DAPPER1 expression had no obviously change after treated with trichostatin A (TSA).Decreased protein expression of DAPPER1 was observed in ESCC tumor tissues compared with non-cancerous tissues (P < 0.01),and associated with the methylation status of this gene (P < 0.01).Conclusion DAPPER1 plays an important role of tumor suppressor gene in esophageal carcinoma,and the aberrant hypermethylation may be one of the main mechanisms in abnormal expression of this gene.

Full text: Available Index: WPRIM (Western Pacific) Language: Chinese Journal: Chinese Journal of Clinical and Experimental Pathology Year: 2017 Type: Article

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Full text: Available Index: WPRIM (Western Pacific) Language: Chinese Journal: Chinese Journal of Clinical and Experimental Pathology Year: 2017 Type: Article