Objective: To study the reversal effect of NVP-BEZ235 on doxorubicin resistance in Burkitt lymphoma RAJI cell line.
Methods: The doxorubicin-resistant cell line was induced by treating RAJI cells with a concentration gradient of doxorubicin. The levels of Pgp, p-AKT, and p-mTOR in cells were detected by Western blot. Cell viability was detected by MTT assay. IC50 was computed by SPSS.
Results: The doxorubicin-resistant Burkitt lymphoma cell line, RAJI/DOX, was established successfully. The expression of Pgp and the phosphorylation levels of AKT and mTOR in RAJI/DOX cell line were both higher than those in RAJI cell line. NVP-BEZ235 downregulated the phosphorylation levels of AKT and mTOR in RAJI/DOX cell line. NVP-BEZ235 inhibited the proliferation of RAJI/DOX cell line, and the effect was obvious when it was cooperated with doxorubicin.
Conclusion: The constitutive activation of PI3K/AKT/mTOR pathway of RAJI/DOX cell line was more serious than RAJI cell line. NVP-BEZ235 reversed doxorubicin resistance of RAJI/DOX cell line by inhibiting the PI3K/AKT/mTOR signal pathway.
题目: NVP-BEZ235逆转伯基特淋巴瘤RAJI细胞阿霉素耐药的研究.
目的: 研究NVP-BEZ23对耐阿霉素细胞株RAJI/DOX的逆转耐药作用。.
方法: 利用浓度梯度法诱导耐阿霉素细胞株RAJI/DOX；Western blot测定各组细胞Pgp、p-AKT、p-mTOR蛋白水平；MTT法检测细胞抑制率，SPSS软件测定IC50。.
结果: 成功诱导出耐阿霉素细胞株RAJI/DOX。耐阿霉素细胞株RAJI/DOX中Pgp、p-AKT、p-mTOR蛋白水平高于亲本细胞RAJI。NVP-BEZ235可引起耐阿霉素细胞株RAJI/DOX中p-AKT、p-mTOR蛋白水平下降。NVP-BEZ235能够抑制耐阿霉素细胞株RAJI/DOX增殖，与阿霉素具有协同作用。.
结论: PI3K/AKT/mTOR通道在耐阿霉素伯基特淋巴瘤细胞中进一步活化；NVP-BEZ235通过抑制PI3K/AKT/mTOR信号通道活化，能够与阿霉素协同抑制伯基特淋巴瘤耐药细胞，逆转伯基特淋巴瘤耐药细胞对阿霉素的耐药性。.
Keywords: NVP-BEZ235； Burkitt lymphoma; doxorubicin-resistance；reversal effect.