Long noncoding RNA UCA1 targets miR-582-5p and contributes to the progression and drug resistance of bladder cancer cells through ATG7-mediated autophagy inhibition

摘要: Background Rently, the incidence of bladder cancer has been on rise. Accumulating researches have conducted to clarify molecular mechanisms and potential therapeutic targets cancer. The present study aims explore regulatory mechanism urothelial carcinoma-associated 1 (UCA1)-miR-582-5p-ATG7 axis in Methods Quantitative real-time polymerase chain reaction was used detect mRNA level. Relative protein expression detected by western blot. wound healing assay transwell were determine migration invasion cells. addtion, luciferase reporter immunohistochemistry performed. Results UCA1 upregulated tissues cells, while depletion shRNA resulted suppression cell proliferation, invasion, migration, drug resistance. Further studies demonstrated that could directly interact with miR-582-5p, there an inverse correlation between miR-582-5p UCA1. In addition, we found ATG7 is a target can be downregulated either overexpression or knockdown. particular, autophagy reduced when introduced. Moreover, vivo experiment further contribution including tumor growth, knockdown inhibit aforementioned activities. Conclusion These results provided evidence for novel interaction network cancer, is, UCA1-miR-582-5p-ATG7-autophagy axis. Our provides new insight into treatment