ERK1/2通路与舌鳞癌细胞Cal-27生物学行为的相关性

Relationships between ERK1/2 Signaling Pathway and Biological Behaviors of TSCC Cal-27 Cells

目的探讨ERK1/2通路对人舌鳞癌Cal-27细胞生物学行为的影响。方法不同浓度ERK1/2通路抑制剂U0126(5、10、20、40μmol/L)作用于Cal-27,分别处理12、24、36、48h。然后用MTT法检测U0126对Cal-27细胞增殖的影响,划痕实验和Transwell小室法分别检测其对Cal-27体外迁移和侵袭的影响,流式细胞术检测其对细胞凋亡和细胞周期的影响。结果不同浓度U0126均能抑制Cal-27的增殖(P<0.05),减弱Cal-27的迁移和侵袭能力(P<0.05);并能诱导细胞凋亡,使S和G2/M期肿瘤细胞比例减少,G0/G1期比例增加(P<0.05)。结论 U0126能通过抑制ERK1/2信号通路,诱导肿瘤细胞凋亡,抑制细胞的增殖、迁移和侵袭,提示ERK1/2信号通路可能是治疗人类恶性肿瘤的一个潜在的靶点。

Objective To investigate the effects of U0126 on the biological behaviors of squamous cell carcinoma of the tongue（TSCC）Cal-27 cells.Methods The Cal-27 cells were treated with different concentrations of U0126（5,10,20 and 40 μmol/L）for 12,24,36 and 48 h.The effect of U0126 on proliferation of Cal-27 cells was measured by using MTT assay.Scratch wound assay and Transwell were used to detect the influence of U0126 on migration and invasion of Cal-27 cells in vitro.Flow cytometry was used to detect cell cycle and apoptosis.Results Different concentrations of U0126 could inhibit the proliferation of Cal-27 cells（P0.05）,attenuate migration and invasion of tumor cells（P0.05）and induce apoptosis of tumor cells,decrease proportion of cells in S and G2/M phases and increase that in G0/G1 phase（P0.05）.Conclusion U0126 can induce tumor cell apoptosis and inhibit cell proliferation,migration and invasion,suggesting that ERK1/2 pathway may be a potent therapeutic target for human cancer.