SU11248对鼻咽癌CNE-2细胞增殖的影响及其机制

The effect and mechanism of SU11248 on proliferation of nasopharyngeal carcinoma cell line CNE-2

目的研究苹果酸舒尼替尼(SU11248)对鼻咽癌细胞CNE-2增殖的影响,并探讨其作用机制。方法用SU11248处理体外培养的鼻咽癌细胞株CNE-2,采用MTT法检测SU11248对CNE-2细胞增殖能力的影响;经2.5μg/mL SU11284作用不同时间后采用实时荧光定量PCR、Western blot法分别检测CNE-2细胞中P27KIP1、cyclin G1 mRNA和蛋白的表达情况。结果 SU11248可抑制CNE-2细胞增殖,且呈时间和剂量依赖性,半数抑制浓度(IC50)约为2.5μg/mL。SU11248作用CNE-2后cyclin G1 mRNA和蛋白呈时间依赖性降低(P<0.05),而P27KIP1mRNA和蛋白呈时间依赖性升高(P<0.05)。结论 SU11248能明显抑制CNE-2细胞增殖,可能通过上调P27KIP1、下调cyclin G1而发挥作用。

Objective To investigate the effect of sunitinib malate （SUl1284） on proliferation of nasopharyngeal carcinoma cell line CNE-2 and explore its mechanism. Methods Nasopharyngeal carcinoma cell line CNE-2 was treated with SU11248 in vitro, and the change in the proliferation of CNE-2 cell line was observed by MTT assay; Real-time fluorescence quantita- tive PCR （FQ-PCR） and Western blotting were used to detect the levels of P27KIPI , cyclin GI mRNA and protein in CNE-2 cells after treated with 2.5 μg/mL SU11284 for different durations. Results SU11248 inhibited the proliferation of CNE-2 cells in a concentration- and time-dependent manner. The 50% inhibiting concentration （IC50） was 2.5 μg/mL. Moreover, SUl1248 treatment concentration-dependently decreased cyclin G1 mRNA and protein expressions （ P 〈 0.05 ）, in contrast, it time- dependently increased P27KIPI mRNA and protein levels （P 〈 0.05）. Conclusion SU11248 may significantly inhibit the prolif- eration of CNE-2 cells through up-regulating P27KIPI and down-regulating cyclin G1.