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Abstract: Objective To investigate the effect and mechanism of Survivin on the proliferationand apoptosis of etoposide resistant small cell lung cancer cell lines. Methods Etoposide resistancesmall cell lung cancer cell lines were constructed in NCI-H82 and NCI-H446 cell lines (NCI-H82 /ER and NCI-H446 / ER), the IC50 and resistance index of NCI-H82 / ER and NCI-H446 / ER weredetermined. qRT PCR and Western blotting assay were used to detect the expression level of Survivinin the cell lines. Survivin siRNA (si-Survivin group) and Survivin siRNA Negative Control (si-NCgroup) were transfected into NCI-H82 / ER and NCI-H446 / ER cells. Cell proliferation was determined by CCK8, apoptosis was determined by flow cytometry, and phosphorylation levels of PI3K,AKT, and mTOR were detected by Western blotting. Results The IC50 of NCI-H82 / ER and NCIH446 / ER were 154. 5 μmol / L and 130. 5 μmol / L, respectively, with resistance indices of 5. 40and 6. 21. Compared with the NCI-H82 and NCI-H446 cells, the NCI-H82 / ER and NCI-H446 / ERcells had significantly increased expression levels of Survivin mRNA and protein ( P < 0. 001 ).Compared with the cells in the si-NC group, NCI-H82 / ER and NCI-H446 / ER cells in the si-Survivin group had significantly reduced proliferation abilities (P< 0. 05), and significantly increased level of apoptosis ( P < 0. 001), and significantly reduced phosphorylation levels of PI3K, AKT, and mTOR (P< 0. 001). Conclusion Inhibiting Survivin can inhibit the PI3K / AKT / mTOR signaling and affect the proliferation and apoptosis of etoposide resistant small cell lung cancer cells.

Key words: Survivin, small cell lung cancer, etoposide, drug resistance