Abstract
We focused on studying the effects of a key miRNA-mRNA axis in bladder urothelial carcinoma (BUC). Firstly, miRNAs and mRNAs differentially expressed in BUC were analyzed. Clinical information in the TCGA database was used for survival analysis, and the regulator of miRNA-93-5p was predicted. miRNA-93-5p and KLF9 mRNA expression were detected by qRT-PCR. Protein level detection and targeting measurement were, respectively, achieved by western blot and dual-luciferase approaches. The proliferative, invasive, and migratory abilities were tested through CCK-8, Transwell, and wound healing methods. Cell apoptosis in each group was detected through flow cytometry. As discovered, miRNA-93-5p level was markedly high in BUC cells while KLF9 expression was remarkably low. miRNA-93-5p overexpression promoted BUC cell abilities. Besides, miRNA-93-5p inhibited KLF9 expression. Furthermore, KLF9 overexpression dramatically attenuated such promotion on cancer cell abilities. On the whole, miRNA-93-5p/KLF9 axis facilitated BUC progression, offering a new potential target for BUC patients.
Highlights
Bladder cancer (BC), a prevalent tumor in the urogenital system, is caused by the overgrowth of bladder mucosa epithelial cells, with high morbidity and low 5-year survival rate [1]
Bladder urothelial carcinoma (BUC) cell line RT4 was seeded into 96-well plates (3 × 105), and 100 nM miR-mimics/miR-NC and KLF9-WT/KLF9MUT plasmids were cotransfected into cells by utilizing Lipofectamine 2000
To explore whether miRNA-93-5p could regulate BUC cells via targeting KLF9, we used RT4 and RT-112 cell lines to construct miR-NC+oe-NC, miR-NC+oe-KLF9, and miRmimics+oe-KLF9. It was shown from qRT-PCR and western blot results that KLF9 mRNA and protein levels were considerably stimulated in the miR-NC+oe-KLF9 group, while those were comparatively decreased in the miR-mimics +oe-KLF9 group (Figures 5(a) and 5(b)), illustrating that miRNA-93-5p repressed KLF9
Summary
Bladder cancer (BC), a prevalent tumor in the urogenital system, is caused by the overgrowth of bladder mucosa epithelial cells, with high morbidity and low 5-year survival rate [1]. To deeply research the underlying molecular mechanism of metastasis and invasion of BUC is essential, thereby providing a novel therapeutic target and increasing patient’s survival rate. Study reported that miRNA-93-5p is ectopically at a high level in breast cancer [14]. A study reported that methylated KLF9 is an independent prognostic factor of breast cancer [17]. Researching the regulation of KLF9 on BUC is helpful for finding a novel prognostic biomarker and developing a new therapeutic method. This work illustrated that miRNA-93-5p was stimulated in BUC and bound KLF9 to aggravate BUC. These results demonstrated the critical impacts miRNA-93-5p performed on BUC
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