被撤回的出版物: Long non-coding RNA UCA1 targets miR-185-5p and regulates cell mobility by affecting epithelial-mesenchymal transition in melanoma via Wnt/beta-catenin signaling pathway (Retracted article. See vol. 795, 2021)

Melanoma is an aggressive skin carcinoma with poor prognosis. Increasing studies have been carried out to investigate effective therapeutic targets for melanoma treatment. This study focuses on the LncRNA UCA1 and its downstream regulated factors. In our present study, UCA1 expression was discovered to be up-regulated while miR-185-5p expression was down-regulated in melanoma tissues and cell lines. We found that miR-185-5p could directly bind to UCA1 at the miRNA recognition site, and there existed a negative relationship between UCA1 and miR-185-5p. Additionally, knockdown of UCA1 was found to suppress cell invasion through inhibiting EMT in melanoma. However, miR-185-5p inhibitor transfection counteracted the inhibitory effect of UCA1 shRNA on cell invasion and EMT, suggesting that UCA1 shRNA suppressed invasion through inhibiting EMT via up-regulating miR-185-5p expression in melanoma. In addition, depletion of UCA1 decreased the expression of beta-catenin and c-myc, indicating that UCA1 shRNA suppressed WM/beta-catenin signaling pathway. Moreover, activation of Wnt/beta-catenin signaling pathway by Lid treatment could abolish the effects of UCA1 shRNA on melanoma cells mobility and EMT. Finally, in vivo experiments revealed that knockdown of UCA1 inhibited tumor growth and invasion via targeting miR-185-5p through Wnt/beta-catenin signaling pathway. In conclusion, our study indicated that the UCA1/miR-185-5p/Wnt/beta-catenin axis might provide a new potential therapeutic strategy for melanoma treatment.