LncRNA miR17HG promotes tumor progression through AXIN2 by sponging miR-144-3p in bladder cancer.

BACKGROUND: Accumulating evidence indicates that long non-coding RNA (lncRNA) miR17HG plays important roles in tumorigenesis in various cancers. However, its underlying effect on bladder cancer (BC) remains to be explored. OBJECTIVE: This study aims to elucidate the function and molecular mechanisms of lncRNA miR17HG in the proliferation and metastasis of BC. METHODS: BC tissues and matched para-cancerous tissues were collected from our hospital. Oncology functional assays, quantitative reverse-transcription polymerase chain reaction, and western blotting were conducted to confirm the role of lncRNA miR17HG in BC development. The interations among lncRNA miR17HG, miR-144-3p and AXIN2 were verified via luciferase reporter assay. Nude mouse subcutaneous tumor models were established to investigate the effect of lncRNA miR17HG on BC tumor growth. RESULTS: LncRNA miR17HG and miR-144-3p were significantly upregulated, while AXIN2 was downregulated in BC tissues. Knockdown of lncRNA miR17HG or inhibition of miR-144-3p suppressed cell proliferation, migration and invasion, whereas miR-144-3p mimic exerted the opposite effects. Mechanistically, lncRNA miR17HG sponged miR-144-3p to regulate the expression of AXIN2. Furthermore, lncRNA miR17HG knockdown effectively suppressed tumor xenograft growth in mice. CONCLUSION: In summary, this study identifies a novel lncRNA miR17HG/miR-144-3p/AXIN2 pathway in BC and demonstrate that this regulatory axis may serve as a promising therapeutic target for BC.