MicroRNA-200c regulates cisplatin resistance by targeting ZEB2 in human gastric cancer cells

This study was specifically designed to confirm the hypothesis that microRNA-200c (miR-200c) affects the development of cisplatin (DDP) resistance in human gastric cancer cells by targeting zinc finger E-box binding homeobox 2 (ZEB2). A total of 50 gastric cancer tissues and their corresponding norm...

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Veröffentlicht in:Oncology reports 2017-07, Vol.38 (1), p.151-158
Hauptverfasser: Jiang, Tao, Dong, Pengfei, Li, Long, Ma, Xiao, Xu, Pei, Zhu, He, Wang, Yanqiu, Yang, Baotong, Liu, Kuangge, Liu, Jinwei, Xue, Juan, Lv, Runzhe, Su, Panke, Kong, Guoqiang, Chang, Yongchao, Zhao, Chonggao, Wang, Lidong
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Sprache:eng
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Zusammenfassung:This study was specifically designed to confirm the hypothesis that microRNA-200c (miR-200c) affects the development of cisplatin (DDP) resistance in human gastric cancer cells by targeting zinc finger E-box binding homeobox 2 (ZEB2). A total of 50 gastric cancer tissues and their corresponding normal adjacent tissue samples were collected. Then, the expression levels of miR-200c and ZEB2 in both gastric cancer specimens and cells were detected using the quantitative real-time reverse transcription-polymerase chain reaction (qRT-PCR) and immunohistochemical methods. A dual‑luciferase reporter gene assay was conducted to evaluate the effect of miR-200c on the 3'-untranslated region (3'UTR) luciferase activity of ZEB2. SGC7901/DDP cells were transfected with miR-200c mimics and ZEB2 siRNA, respectively. Subsequently, changes in cellular proliferation and apoptosis were detected through the methyl thiazolyl tetrazolium assay and flow cytometric analysis, respectively. We also carried out a western blot analysis assay in order to detect the expression of apoptosis-related genes and ZEB2. miR-200c was significantly downregulated and ZEB2 was significantly upregulated in both gastric cancer tissues and SGC7901/DDP cells when compared with those in normal tissues and SGC7901 cells (P
ISSN:1021-335X
1791-2431
DOI:10.3892/or.2017.5659