分子生物学
IVD分子诊断
细胞培养与分析
蛋白研究
细胞因子
重组蛋白
抗体
高通量测序建库
病原检测UCF系列
生物医药
工具酶
抑制剂激活剂与常用试剂
仪器
耗材

Effects of paclitaxel combined with miR-448 on growth and proliferation of bladder cancer EJ cells.

Wang Y, Li LJ, Qiu MX, Gong BS

Journal:European Review for Medical and Pharmacological Sciences

IF:2.39

DOI:10.26355/eurrev_201806_15157

PMID:29917187

Published:2018-06-01

research field:肿瘤学分子生物学药理学

Abstract

Objective Bladder cancer is one of the most common malignant tumors of the urinary system characterized by a high recurrence rate after treatment. Paclitaxel is a new type of anti-neoplastic agent used for treatment by inhibiting the proliferation of bladder cancer cells. This study aimed to explore the mechanism of paclitaxel on the inhibition of bladder cancer cell proliferation by applying paclitaxel combined with miR-448 on bladder cancer cells. Materials and methods Bladder cancer EJ cells were divided into 5 groups, including control group, paclitaxel group, negative control (NC) group, microRNA-448 (miR-448) mimic group, and paclitaxel combined with miR-448 mimic group. Cell apoptosis was tested by flow cytometry. Cell proliferation was determined by cell counting kit 8 (CCK8) assay. The regulation of miR-448 on B cell lymphoma 2 (Bcl-2) gene was assessed by dual luciferase reporter assay. Bcl-2 protein expression was detected by Western blot. Results The apoptotic rate of cells was significantly increased, while the cell proliferation ability was significantly reduced in paclitaxel group and miR-448 mimic group compared with control (p<0.05). Cell apoptotic rate in paclitaxel combined with miR-448 mimic group was markedly higher than that of paclitaxel group (p<0.05). MiR-448 can bind to the 3'UTR region of Bcl-2 mRNA and regulate the expression of Bcl-2. The expression of Bcl-2 protein in paclitaxel group and miR-448 mimic group was significantly lower than that in control group and higher than paclitaxel combined with miR-448 mimic group (p<0.05). Conclusions Paclitaxel combined with miR-448 promoted EJ cell apoptosis and inhibited cell proliferation by suppressing Bcl-2 gene expression.

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