[High expression of miR-204-5p promotes malignant behaviors of bladder cancer cells by negatively regulating RAB22A].

L Li, Y Guo, C Wang, R Chang, W Sun, W Gao, C Wang, B Liu
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引用次数: 0

Abstract

Objective: To explore the regulatory effect of miR-204-5p on biological behaviors of bladder cancer cells and its molecular mechanism.

Methods: Survival analysis and correlation analysis were performed using TCGA database to explore the association of miR-204-5p expression with survival outcomes and clinicopathological parameters of bladder cancer patients. The expression level of miR-204-5p was detected in bladder cancer and adjacent tissues and in normal uroepithelial cells and bladder cancer cells. In cultured bladder cancer cells, the effects of miR-204-5p overexpression and knockdown on cell proliferation, migration, invasion, and apoptosis were analyzed. Transcriptome sequencing, bioinformatics analysis and dual-luciferase assay were carried out to confirm targeted inhibition of RAB22A by miR-204-5p to promote malignant biological behaviors of bladder cancer cells.

Results: Patients with high miR-204-5p expressions had lowered median survival time and poor prognosis (P < 0.05). The expression of miR-204-5p was significantly up-regulated in bladder cancer tissues and cells (P < 0.05). In bladder cancer cells, miR-204-5p overexpression significantly promoted cell proliferation, migration and invasion and reduced cell apoptosis. Transcriptome sequencing, bioinformatics analysis and dual-luciferase assay all suggested that RAB22A was a key downstream factor of miR-204-5p. Overexpression of miR-204-5p significantly inhibited RAB22A expression in bladder cancer cells, and overexpression of RAB22A partially reversed miR-204-5p overexpression-induced enhancement of bladder cancer cell proliferation.

Conclusion: High expression of miR-204-5p promotes proliferation, migration and invasion and reduces apoptosis of bladder cancer cells by negatively regulating RAB22A expression.

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[高表达miR-204-5p通过负调控RAB22A促进膀胱癌细胞的恶性行为]。
目的:探讨miR-204-5p对膀胱癌细胞生物学行为的调控作用及其分子机制。方法:采用TCGA数据库进行生存分析和相关性分析,探讨miR-204-5p表达与膀胱癌患者生存结局及临床病理参数的关系。检测miR-204-5p在膀胱癌及癌旁组织、正常尿上皮细胞和膀胱癌细胞中的表达水平。在培养的膀胱癌细胞中,分析miR-204-5p过表达和敲低对细胞增殖、迁移、侵袭和凋亡的影响。通过转录组测序、生物信息学分析和双荧光素酶测定证实miR-204-5p靶向抑制RAB22A促进膀胱癌细胞的恶性生物学行为。结果:miR-204-5p高表达患者中位生存时间较短,预后较差(P < 0.05)。miR-204-5p在膀胱癌组织和细胞中的表达明显上调(P < 0.05)。在膀胱癌细胞中,miR-204-5p过表达可显著促进细胞增殖、迁移和侵袭,减少细胞凋亡。转录组测序、生物信息学分析和双荧光素酶检测均提示RAB22A是miR-204-5p的关键下游因子。miR-204-5p过表达可显著抑制膀胱癌细胞中RAB22A的表达,RAB22A过表达可部分逆转miR-204-5p过表达诱导的膀胱癌细胞增殖增强。结论:高表达miR-204-5p通过负调控RAB22A表达促进膀胱癌细胞增殖、迁移和侵袭,减少膀胱癌细胞凋亡。
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来源期刊
南方医科大学学报杂志
南方医科大学学报杂志 Medicine-Medicine (all)
CiteScore
1.50
自引率
0.00%
发文量
208
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