Abstract
The present investigation was intended to elucidate whether long noncoding RNA small nuclear RNA host gene 16 (SNHG16) could regulate the epithelial-mesenchymal transition process of bladder cancer cells by directing expressions of miR-17-5p and metalloproteinases 3 (TIMP3). To elucidate the point, we collected 275 pairs of bladder cancer tissues and corresponding adjacent normal tissues, as well as four bladder cancer cell lines and the normal human bladder epithelial cell line. Moreover, pcDNA3.1-SNHG16, si-SNHG16, miR-17-5p mimic, miR-17-5p inhibitor, pcDNA3.1-TIMP3, and si-TIMP3 were prepared for transfection, and CCK-8 assay, colony formation assay, flow cytometry, wound healing assay, and transwell assay were carried out. Finally, the dual luciferase reporter gene assay was performed to figure out whether targeted regulations were present among SNHG16, miR-17-5p, and TIMP3. The laboratory findings demonstrated that the bladder cancer patients carrying under-expressed SNHG16 or miR-17-5p were associated with extended survival time when compared with those possessing overexpressed SNHG16 and miR-17-5p (P < 0.05). Furthermore, overexpression of SNHG16 and miR-17-5p both enhanced the viability, proliferation, migration, and invasion (P < 0.05), and simultaneously suppressed their apoptosis (P < 0.05). Transfections of pcDNA3.1-SNHG16 and si-SNHG16, respectively, resulted in overexpression and under-expression of miR-17-5p, and the dual luciferase reporter gene assay demonstrated a targeted relationship between SNHG16 and miR-17-5p (P < 0.05). Besides, the expression of TIMP3 was subjected to targeted regulation of miR-17-5p (P < 0.05), and its overexpression could reverse the effects of miR-17-5p on proliferation and metastasis (P < 0.05). Conclusively, purposeful modification of SNHG16/miR-17-5p/TIMP3 signaling might be conducive to postpone the aggravation of bladder cancer.