Backgrounds/Aims: Long non-coding RNA (lncRNA) X-inactive specific transcript (XIST) is involved in the progression of several tumors. The interaction between lncRNA and miRNA or miRNA’s target genes is reported to play crucial roles in malignancy. In addition, Androgen receptor (AR) is considered to be involved in bladder cancer progression. In this study, we investigated the role of XIST in human bladder cancer and its interaction with miR-124 and AR. Methods: XIST and AR expression was detected in bladder tumor samples and cell lines. Effects of XIST and AR on bladder cancer cells growth, invasion and migration were analyzed. Bioinformatic analysis and luciferase assays were used to identify the interaction among XIST, AR and miR-124. The correlations of miR-124 with XIST and AR in bladder cancer samples were statistically analyzed. Results: XIST and AR were upregulated in bladder cancer tissues and positively correlated. Higher XIST and AR expression were related to poorer TNM stage of bladder cancer. XIST knockdown reduced bladder cancer cells’ proliferation, invasion and migration. While this inhibitory effect could be partially restored by AR overexpression. XIST inhibited miR-124 expression by directly targeting. Moreover, miR-124 could bind to the 3’UTR of AR to regulate its expression. MiR-124 inhibition partially restored the XIST knockdown-induced reduction of AR, c-myc, p27, MMP13 and MMP9 expression. In bladder cancer tissues, miR-124 level was inversely correlated with the expression of XIST and AR, respectively. Conclusion: These findings indicated that XIST might be an oncogenic lncRNA that promoted the bladder cancer growth, invasion and migration via miR-124 dependent AR regulation.

Background: Invasive bladder tumors cause a worse prognosis in patients and remain a clinical challenge. Epithelial–mesenchymal transition (EMT) is associated with bladder cancer metastasis. In the present research, we attempted to demonstrate a novel mechanism by which a long noncoding RNA (lncRNA)-miRNA-mRNA axis regulates EMT and metastasis in bladder cancer. Methods: Immunofluorescence (IF) staining was used to detect Vimentin expression. The protein expression of ZEB1, Vimentin, E-cadherin, and Snail was investigated by using immunoblotting assays. Transwell assays were performed to detect the invasive capacity of bladder cancer cells. A wound healing assay was used to measure the migratory capacity of bladder cancer cells. Results: Herein, we identified lncRNA VIM-AS1 as a highly- expressed lncRNA in bladder cancer, especially in metastatic bladder cancer tissues and high-metastatic bladder cancer cell lines. By acting as a ceRNA for miR-655, VIM-AS1 competed with ZEB1 for miR-655 binding, therefore eliminating the miR-655-mediated suppression of ZEB1, finally promoting EMT in both high- and low-metastatic bladder cancer cells and enhancing cancer cell metastasis. Conclusions: In conclusion, the VIM-AS1/miR-655/ZEB1 axis might be a promising target for improving bladder cancer metastasis via an EMT-related mechanism.

MicroRNA‑145 (miR‑145) and long non‑coding RNA (lncRNA) growth arrest specific 5 (GAS5) function as tumor suppressors in prostate carcinoma. The aim of the present study was to investigate the role of miR‑145 and lncRNA GAS5 in prostate carcinoma. In the present study, miR‑145 and lncRNA GAS5 expression levels were demonstrated to be downregulated in tumor tissues compared with adjacent healthy tissues of patients with prostate carcinoma. miR‑145 and lncRNA GAS5 expression levels were found to be positively and significantly correlated in tumor tissues, but not in adjacent healthy tissues. A follow‑up study revealed that low miR‑145 and lncRNA GAS5 expression levels were associated with poor survival. Overexpression of miR‑145 resulted in upregulated lncRNA GAS5, whereas lncRNA GAS5 overexpression or silencing did not affect miR‑145 expression. Overexpression of miR‑145 and lncRNA GAS5 promoted apoptosis and inhibited cell proliferation in prostate carcinoma cell lines, whereas lncRNA GAS5 knockdown had an opposite effect. In addition, lncRNA GAS5 knockdown partially attenuated the effect of miR‑145 overexpression of cancer cell proliferation and apoptosis. Therefore, miR‑145 may inhibit cell proliferation and induce apoptosis in human prostate carcinoma by upregulating lncRNA GAS5.