艾塞那肽对人舌鳞癌SCC-25细胞增殖、侵袭及凋亡的影响

摘要： 目的 探讨艾塞那肽对人舌鳞癌 SCC-25 细胞增殖、 侵袭能力以及凋亡相关指标的影响。方法 体外培养 SCC-25 细胞， Western blot 检测 SCC-25 细胞中胰高血糖素样肽 1 受体（GLP-1R）表达。实验分 4 组： 对照组、 1、 10 和 100 nmol/L 艾塞那肽处理组。培养 24 h、 48 h 和 72 h 后 MTT 法检测各组细胞增殖能力， Transwell 实验检测各组细胞侵袭能力。Western blot 检测基质金属蛋白酶（MMP） -2、 Caspase-3 和 p38 丝裂原活化蛋白激酶（Phosphop38 MAPK）表达。结果 SCC-25 细胞表达 GLP-1R。与对照组相比， 艾塞那肽处理组细胞存活率及侵袭率明显降低（P < 0.05）， MMP-2 蛋白表达降低（P < 0.05）， Caspase-3 蛋白表达明显升高（P < 0.05）； 各指标变化呈现艾塞那肽浓度和时间依赖性。10 nmol/L 艾塞那肽处理组 24 h 后 Phospho-p38 MAPK 表达升高（P < 0.05）。结论 艾塞那肽可抑制 SCC-25 细胞增殖和侵袭， 且可能通过促进 Phospho-p38 MAPK 和 Caspase-3 的表达诱导细胞凋亡。

Effects of exenatide on the cell proliferation,invasion and apoptosis of human tongue squamous cell carcinoma SCC-25

Abstract: Objective To detect the effects of exenatide on the related indicators of proliferation, invasion and apopto? sis of cell line SCC-25. Methods SCC-25 cells were cultured in vitro. The expression level of glucagon like peptide 1 re? ceptor (GLP-1R) was determined by Western blot assay in SCC-25 cells. SCC-25 cells were divided into four groups: con? trol group and exenatide group (1, 10 and 100 nmol/L). The ability of cell proliferation was detected using MTT assay after 24 h, 48 h and 72 h of culture. The ability of invasion was measured with Transwell assays. The expression levels of MMP- 2, Caspase-3 and Phospho-p38 MAPK were measured by Western blot assay. Results GLP-1 receptor expression was found in SCC-25 cells. Compared with control group, the cell survival rate, invasion rate and the expression of MMP-2 were signifi? cantly decreased in SCC-25 group (P < 0.05). The expression of Caspase-3 were significantly increased (P < 0.05).Changes were in a concentration-dependent and time-dependent manner (P < 0.05). The expression of Phospho-p38 MAPK was sig? nificantly increased at 24 h in 10 nmol/L exenatide group (P < 0.05). Conclusion Exenatide can inhibit the cell prolifera? tion and invasion, which may contribute the apoptosis by promoting expressions of Phospho-p38 MAPK and Caspase-3 of SCC-25 cells.