Long non-‑coding RNA SNHG16 functions as a tumor activator by sponging miR‑373‑3p to regulate the TGF‑β‑R2/SMAD pathway in prostate cancer

Long non‑coding RNAs (lncRNAs) are involved in the pathogenesis of prostate cancer (PCa) as competitive endogenous RNA. The present study aimed to investigate the molecular mech--anisms of lncRNA small nucleolar RNA host gene 16 (SNHG16) in the proliferation and metastasis of PCa cells. Cancer tissues and adjacent normal tissues were collected from 80 patients with PCa who did not receive any treatment. Reverse transcription‑quantitative PCR analysis was performed to detect the expression levels of SNHG16, hsa‑microRNA (miRNA/miR)‑373‑3p and transforming growth factor‑β receptor type 2 (TGF‑β‑R2), and Spearman's correlation coefficient analysis was performed to assess the correlations between these molecules. Furthermore, the effects of SNHG16 knockdown and overexpression on the biological functions of DU‑145 PCa cells and TGF‑β‑R2/SMAD signaling were analyzed. The dual‑luciferase reporter assay was performed to assess the associations between SNHG16 and miR‑373‑3p, and TGF‑β‑R2 and miR‑373‑3p, the effects of which were verified via rescue experiments. The results demonstrated that the expression levels of SNHG16 and TGF‑β‑R2 were significantly upregulated in PCa tissues, whereas miR‑373‑3p expression was significantly downregulated (P