LncRNA HMGA2-AS1 promotes postoperative recurrence in non-muscle-invasive bladder cancer by sponging miR-367-3p to activate YAP1.

BACKGROUND

Non-muscle-invasive bladder cancer (NMIBC) is characterized by a high postoperative recurrence rate. LncRNAs have emerged as key regulators in cancer progression. The clinical relevance and mechanistic role of HMGA2-AS1 in NMIBC recurrence remain unclear.

METHODS

Clinical samples contained paired adjacent and tumor tissues from 110 NMIBC patients. HMGA2-AS1 expression was examined using qRT-PCR, and its association with clinicopathological features and recurrence-free survival (RFS) was analyzed. Kaplan-Meier and Cox regression analyses were performed to evaluate prognostic value. Functional assays, including CCK-8, migration, and stemness- and epithelial-mesenchymal transition-related gene expression analyses, were conducted in RT4 and 5637 cells. RNA interaction analyses were performed using a dual-luciferase reporter assay.

RESULTS

HMGA2-AS1 was elevated in NMIBC tissues and was closely associated with adverse clinicopathological characteristics (tumor grade and stage), and shorter RFS. HMGA2-AS1 is an independent risk factor for postoperative recurrence. Functionally, HMGA2-AS1 silencing suppressed cell proliferation, migration, stemness, and EMT in vitro. HMGA2-AS1 acted as a molecular sponge for miR-367-3p, thereby relieving repression of YAP1. Rescue experiments confirmed that inhibition of miR-367-3p or restoration of YAP1 expression reversed the influence of HMGA2-AS1 knockdown.

CONCLUSION

HMGA2-AS1 is upregulated in NMIBC. HMGA2-AS1 promotes NMIBC progression through the miR-367-3p/YAP1 axis.