Abstract: Objective To investigate the effect of salidroside (SAL) on the proliferation, apoptosis and epithelial mesenchymal transformation (EMT) of non-small cell lung cancer (NSCLC) cell line and to clarify the molecular mechanism. Methods The cancer tissues from 22 lung cancer patients and adjecent tissues were collected, and the different lung cancer cell lines (A549, H358, H1299, H1650) were cultured in vitro. RT-qPCR was used to detect the expression of transforming acidic coiled-coid protein 2(TACC2) in cancer tissues and the lung cancer cell lines. After cells (A549 and H1299) were treated with SAL at different concentrations, the apoptosis and proliferation rates were analyzed by flow cytometry and CCK-8, respectively. The expression of E-cadherin, N-cadherin, TACC2 and the phosphorylation level of P38/MAPK in NSCLC cell were detected by Western blot. Plasmid (pcDNA3.0-TACC2) was transfected into A549 and H1299 cell to detect the effects of TACC2 over-expression on the levels of apoptosis, proliferation and EMT. Results The relative expression of TACC2 in lung cancer tissue significantly increased as compared with adjecent tissues.Meanwhile, the expression of TACC2 in NSCLC cell was also markedly higher than human lung fibroblasts cell line(HFL-1)(P＜0.05). Different concentrations of SAL can significantly inhibit the proliferation and increase the apoptosis of cells(P＜0.05). Western blot results showed that the expression of TACC2 and N-cadherin was significantly down-regulated, while E-cadherin expression was up-regulated in A549 and H1299 cells after treatment with SAL. Transfection with pcDNA3.0-TACC2 plasmid could significantly reduced the inhibited effect of SAL on the proliferation and EMT of A549 and H1299 cells (P＜0.05). In addition, the phosphorylation of intracellular p38/MAPK was significantly reduced after treatment with various SAL concentrations (P＜0.05). Conclusions SAL can inhibit the levels of proliferation and EMT in NSCLC cell by negatively regulates the expression of TACC2, which may be related to the inhibition of p38/MAPK signaling pathway.

Key words: salidroside, transforming acidic coiled-coil protein 2(TACC2), non-small cell lung cancer, proliferation, epithelial mesenchymal transformation