Abstract:Objective: To study the effect of long non coding RNA human microRNA17 cluster host gene (LncRNA MIR17HG) on the malignant biological behavior of bladder cancer (BCa) cells by targeting microRNA (miR)-130a-3p. Methods: RT-qPCR was used to measure LncRNA MIR17HG and miR-130a-3p in human urinary tract epithelial cells SV-HUC-1 and human BCa cells (T24, UM-UC-3, 5637). Dual luciferase assay report was used to detect the relationship between LncRNA MIR17HG and miR-130a-3p. BCa cells T24 were studied and assigned into Con group, sh-NC group, sh-lncRNA MIR17HG group, sh-lncRNA MIR17HG+NC inhibitor group, and sh-lncRNA MIR17HG+miR-130a-3p inhibitor group. RT-qPCR method was used to test LncRNA MIR17HG and miR-130a-3p. CCK8, cell scratch, Transwell, flow cytometry, and Western blot experiments were used to detect cell proliferation, migration, invasion, apoptosis, and related proteins in each group. Results: In human BCa cells, the LncRNA MIR17HG increased and miR-130a-3p decreased (P<0.05); the difference between the two was most clear in T24 cells, so T24 cells were selected for the experiment. In the dual luciferase reporter results, the WT lncRNA MIR17HG+miR-130a-3p mimic group showed lower luciferase activity than the WT lncRNA MIR17HG+mimic-NC group (P<0.05). For Con group and sh-NC group, the sh-LncRNA MIR17HG group showed decreases in LncRNA MIR17HG, survival rate, invasion number, scratch healing rate, PCNA, and N-cadherin in T24 cells, and increases in miR-130a-3p, apoptosis rate, cleaved caspase-3, and E-cadherin (P<0.05). For sh-lncRNA MIR17HG group and sh-lncRNA MIR17HG+NC inhibitor group, the sh-lncRNA MIR17HG+miR-130a-3p inhibitor group showed no clear changes in LncRNA MIR17HG in T24 cells, increases in survival rate, invasion number, scratch healing rate, PCNA, and N-cadherin in T24 cells, and decreases in miR-130a-3p, apoptosis rate, cleaved caspase-3, and E-cadherin (P<0.05). Conclusion: Knockdown of LncRNA MIR17HG may inhibit the malignant biological behavior of BCa cells by targeting upregulation of miR-130a-3p.