Li L, Guo Y, Wang C, Chang R, Sun W, Gao W, Wang C, Liu B
Department of Urology, First Affiliated Hospital of Bengbu Medical University, Bengbu 233004, China.
Department of Anesthesiology, Bozhou People's Hospital, Bozhou 236000, China.
Nan Fang Yi Ke Da Xue Xue Bao. 2024 Nov 20;44(11):2235-2242. doi: 10.12122/j.issn.1673-4254.2024.11.21.
To explore the regulatory effect of miR-204-5p on biological behaviors of bladder cancer cells and its molecular mechanism.
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.
Patients with high miR-204-5p expressions had lowered median survival time and poor prognosis ( < 0.05). The expression of miR-204-5p was significantly up-regulated in bladder cancer tissues and cells ( < 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.
High expression of miR-204-5p promotes proliferation, migration and invasion and reduces apoptosis of bladder cancer cells by negatively regulating RAB22A expression.
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。
利用TCGA数据库进行生存分析和相关性分析，以探讨miR-204-5p表达与膀胱癌患者生存结局及临床病理参数的关联。检测膀胱癌及癌旁组织、正常尿路上皮细胞和膀胱癌细胞中miR-204-5p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。进行转录组测序、生物信息学分析和双荧光素酶测定，以证实miR-204-5p对RAB22A的靶向抑制作用促进膀胱癌细胞的恶性生物学行为。
miR-204-5p高表达患者的中位生存时间缩短，预后较差（<0.05）。miR-204-5p在膀胱癌组织和细胞中的表达显著上调（<0.05）。在膀胱癌细胞中，miR-204-5p过表达显著促进细胞增殖、迁移和侵袭，并减少细胞凋亡。转录组测序、生物信息学分析和双荧光素酶测定均表明RAB22A是miR-204-5p的关键下游因子。miR-204-5p过表达显著抑制膀胱癌细胞中RAB22A的表达，而RAB22A过表达部分逆转了miR-204-5p过表达诱导的膀胱癌细胞增殖增强。
miR-204-5p高表达通过负调控RAB22A表达促进膀胱癌细胞的增殖、迁移和侵袭，并减少其凋亡。
