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目的:探讨TGF-β1在腺样囊性癌的增殖、迁移和侵袭、浸润过程中的作用和相关机制。方法:以腺样囊性癌ACC-2细胞株为研究对象,采用TGF-β1刺激ACC-2细胞,MTT法检测ACC-2细胞的增殖能力,Transwell实验检测细胞迁移、侵袭能力,Western蛋白印迹检测ACC-2细胞MAPK(P38、JNK、ERK)的活化及MMP-2表达的变化,实时定量PCR检测ACC-2细胞中MMP-2的mRNA表达变化。采用SPSS17.0软件包对数据进行统计学分析。结果:TGF-β1刺激后,ACC-2细胞增殖能力无显著变化(P>0.05),但迁移、侵袭能力增强(均为P<0.01);同时,ACC-2细胞p-ERK1/2、p-P38和MMP-2蛋白表达升高(均为P<0.05),MMP-2 mRNA表达亦升高(P<0.01),但p-JNK1/2蛋白无显著变化(P>0.05)。结论:TGF-β1可增强人唾液腺腺样囊性癌ACC-2细胞的迁移和侵袭能力,活化p-ERK1/2和p-P38,上调MMP-2的表达。TGF-β1/MAPK/MMP-2通路可能参与人唾液腺腺样囊性癌ACC-2细胞侵袭能力的调节。
Objective: To investigate the role and mechanism of TGF-β1 in the proliferation, migration, invasion and invasion of adenoid cystic carcinoma. Methods: ACC-2 cells were treated with TGF-β1 and the proliferation of ACC-2 cells was detected by MTT assay. The migration and invasion of ACC-2 cells were detected by Western blot The activation of MAPK (P38, JNK, ERK) and the expression of MMP-2 in ACC-2 cells were detected. The mRNA expression of MMP-2 in ACC-2 cells was detected by real- SPSS17.0 software package for statistical analysis of the data. Results: The proliferation of ACC-2 cells was not affected by TGF-β1 (P> 0.05), but the ability of invasion and migration was enhanced (all P <0.01). Meanwhile, the expression of p-ERK1 / (P <0.05). The mRNA expression of MMP-2 also increased (P <0.01), but there was no significant change in p-JNK1 / 2 protein (P> 0.05). CONCLUSION: TGF-β1 can enhance the migration and invasion of human salivary adenoid cystic carcinoma ACC-2 cells, activate p-ERK1 / 2 and p-P38 and up-regulate the expression of MMP-2. The TGF-β1 / MAPK / MMP-2 pathway may be involved in the regulation of invasiveness of human salivary adenoid cystic carcinoma ACC-2 cells.