细胞生长
核糖核酸
长非编码RNA
下调和上调
癌基因
免疫沉淀
细胞培养
细胞
细胞生物学
生物
细胞凋亡
分子生物学
癌症研究
化学
基因
细胞周期
遗传学
作者
Feng Feng,Jing Yang,Aiping Chen,Meng Cui,Lianjun Li
摘要
Increasing evidences have suggested that long non-coding RNAs are critical regulators in the progression of tumor growth. Long intergenic non-protein coding RNA 1232 (LINC01232) was verified as an oncogene in multiple cancers. Nevertheless, its function in bladder cancer (BC) remains to be uncovered. In the current study, we detected LINC01232 expression utilizing quantitative real-time polymerase chain reaction (RT-qPCR) and discovered that LINC01232 was overexpressed in BC cell lines versus normal cell line. Besides, the effect of LINC01232 on BC cell behaviors was measured by colony formation, Cell Counting Kit-8 (CCK-8), transwell, TdT-mediated dUTP Nick-End Labeling and caspase-3/8 activity assays. Functionally, LINC01232 deficiency suppressed cell proliferation, migration and invasion. Next, miR-370-5p was proved to bind with LINC01232 by RNA pull down, RNA-binding protein immunoprecipitation (RIP) and luciferase reporter assays. Furthermore, PIM3 expression was negatively modulated by miR-370-5p and markedly increased in BC cell lines. Moreover, PIM3 silence repressed proliferation, migration and invasion but triggered apoptosis of BC cells. The rescue assays validated that upregulation of PIM3 recovered the effects of LINC01232 silence on the growth of BC cells. To summarize, our study manifested that LINC01232 accelerates BC progression by targeting miR-370-5p/PIM3 axis. Targeting LINC01232 might offer novel insight into BC treatment.
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