Abstract
The long noncoding RNA cancer susceptibility candidate 9 (CASC9) has been revealed to be an oncogenic gene in several types of cancer, and high CASC9 expression is related to tumorigenesis and cancer progression. However, the role of CASC9 in bladder cancer (BC), particularly during epithelial‑mesenchymal transition (EMT), has not been characterized. RT‑qPCR, EdU, CCK‑8, wound scratch, Transwell and flow cytometric assays were performed to detect CASC9 expression, miR‑758‑3p expression and their functions in BC. RNA FISH was used to detect CASC9 subcellular localization. Luciferase reporter assay, RT‑qPCR assay and western blotting were used to explore the relationship of CASC9, miR‑758‑3p and TGF‑β2. In the present study, it was revealed that CASC9 regulated EMT in BC. CASC9 expression was significantly upregulated in BC cell lines and specimens compared to that in adjacent normal bladder tissues. Upregulated CASC9 was associated with increased invasion ability and poor prognosis of BC. CASC9 knockdown inhibited BC cell proliferation, migration and invasion. Furthermore, a bioinformatics study and luciferase reporter assays revealed that CASC9 functioned as a ceRNA for miR‑758‑3p. CASC9 inhibited microRNA (miR)‑758‑3p activity and resulted in the de‑suppression of its target transforming growth factor (TGF)‑β2. TGF‑β signaling driven by TGF‑β2 was crucial for CASC9 to promote EMT in BC. Collectively, these results indicated that CASC9 sponged miR‑758‑3p to regulate the expression of TGF‑β2, which activated the TGF‑β signaling pathway and promoted proliferation and EMT in BC.