Propofol Accelerates Lung Cancer Cells Apoptosis Through Regulation Of Rno-Mir-665 And Bclxl Expression

Background: Non-small-cell lung cancer is the leading cause of cancer-related mortality in human worldwide. Propofol is widely used in general anesthesia and sedation, which is also well-known for its anti-tumor function in many cancer cells. Methods: Cck8 assay was used for cell proliferation test; Flow cytometer, TUNEL assay and caspase-3 activity analysis were used for cell apoptosis. After transfected with rno-miR-665 mimics or inhibitor in A549 cells, the functions of proliferation and apoptosis was investigated. Quantitative polymerase chain reaction analysis and western blot were performed to detect the expression of related proteins in A549 cells. The target gene of rno-miR-665 was determined by luciferase assay and Western blot. Results: Propofol inhibited A549 cell proliferation and induced cell apoptosis significantly in vitro. Introduction of rno-miR-665 mimics apparently suppressed the proliferation and induced apoptosis of A549 cells, while transfection with rno-miR-665 inhibitor in A549 cells contributed to propofol not alter cell proliferation and apoptosis. Moreover, luciferase reporter assay identified the 3'-UTR of bcl-xl mRNA contained a complementary sequence for rno-miR-665. Bcl-xl was a direct target of rnomiR-665. Conclusion: Propofol inhibits proliferation and induces apoptosis of A549 cells through, at least partly, regulation of rno-miR-665. Our study provided a better understanding of propofol function in NSCLC cells.