Linc-smad７ 通过靶向 miR-125b/SIRT1 轴 促进胰腺癌细胞迁移和侵袭

Objective To explore the role of long non-coding RNA smad7 (Linc-smad7) in invasion and migration of pancreatic cancer (PC) cells and its mechanisms. Methods The expression level of Linc-smad7 in PC tissues and cell lines was detected by qRT-PCR assays. Transwell assays were performed to observe the effect of Linc-smad7 overexpression on the migration and invasion abilities of PaCa-2 cells. Luciferase reporter analysis was made to detect the direct binding effect of Linc-smad7 on miR-125b and miR-125b on Sirtuinl(SIRTl). qRT-PCR assays were used to detect the regulatory effect of Linc-smad7 on miR-125b expression in PaCa-2 cells. qRT-PCR and Western blotting assays were used to detect the regulatory effect of miR-125b on SIRT1 expression. Results Linc-smad7 was significantly increased in PC tissues and cell lines. Paca-2 cells with overexpressed Linc-smad7 showed higher migration and invasion abilities, while miR-125b expression was decreased. After the expression of miR-125b was increased, the expression of SIRT1 was decreased significantly. Luciferase reporter assays results suggested that Linc-smad7 directly targeted with miR-125b, and miR-125b directly bound with SIRT1. Increased Linc-Smad7 or decreased miR-125b could reverse the effect of SIRT1 inhibition on invasion and migration of PaCa-2 cells. Conclusion Linc-smad7 promotes invasion and migration of PaCa-2 cells through miR-125b/SIRTl axis.