Background
Long non-coding RNA-urothelial carcinoma associated 1 (LncRNA-UCA1) is a crucial oncogene that is deregulated in many types of cancers. However, the mechanism of UCA1 function, especially for its posttranscriptional regulation in lung cancer, remains unclear.
Conclusions
Our results demonstrated that miR-138 and miR-193 affect cell function by directly targeting and regulating UCA1 in lung cancer.
Methods
miRCode was used to predict potential miRNA candidates that might target UCA1. The targets of miR-138 and miR-193 on UCA1 and CDK6 were verified by luciferase reporter analysis. Western blotting was used to detect protein levels. The RNA level was evaluated using quantitative real-time polymerase chain reaction (PCR). Proliferation, wound healing, and transwell invasion assays were performed to assess cell proliferation and invasion abilities. Correlations between miR-138 or miR-193 and UCA1 in lung cancer tissues was assessed using quantitative real-time PCR.
Results
miR-138 and miR-193 specifically targeted and regulated lncRNA-UCA1. MiR-138 and miR-193 both suppressed cell proliferation and cell cycle progression. Moreover, miR-138 and miR-193 inhibited cell migration and invasion. Overexpression of UCA1 reversed the proliferation, migration, and invasion suppression effects of miR-138 or miR-193. Furthermore, miR-138/193 affected the expression of UCA1 downstream genes. UCA1 regulated the expression of CDK6 as a miR-138 and miR-193 common target. In human lung cancer tissues, our study showed a significant negative correlation between miR-138 or miR-193 and UCA1 in lung cancer tissues. Conclusions: Our results demonstrated that miR-138 and miR-193 affect cell function by directly targeting and regulating UCA1 in lung cancer.