50值為(2.06±0.38)μmol / L,能夠誘導細胞產生凋亡小體和DNA ladder。流式細胞檢測到了細胞凋亡峰,并觀察到細胞周期出現(xiàn)S/G2+M期阻滯。Western-blot結果顯示P-gp表達降低,并且觀察到CIP-36可破壞KBV 200細胞的細胞骨架。結論:CIP-36可能通過降低P-gp的表達,破壞細胞骨架等多靶點克服KBV 200細胞株的多藥耐藥性。;Objective: To study the antitumor activity of CIP-36 on multidrug resistance human oral squamous carcinoma cells (KBV 200 cells) in vitro and the feasible anticancer mechanisms. Methods: MTT assay, morphological study, DNA gel electrophoresis, flow cytometry, western-blot, and immunofluorescence were carried out. Results: The IC50 value of CIP-36 on KBV 200 cells was (2.06 ± 0.38) μmol / L. After treated with CIP-36, the apparent morphological characteristic and typical DNA ladder of KBV 200 cells were all detected. Both the number of apoptosis cells and the cell cycle were measured by flow cytometric; A typical “Sub-G1 peak” was checked and CIP-36 blocked the cell cycle at S/G2 + M phase. Western-blot showed that the expression of P-glycoprotein was decreased. CIP-36 could interfere with microtubule polymerization and disrupt cytoskeleton. Conclusions: CIP-36 has the potentiality to overcome P-glycoprotein- mediated multidrug resistance in the KBV 200 cell line."/>