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目的:探讨炎症因子白细胞介素6(IL-6)对胆囊癌细胞生物学行为的影响及其与JAK/STAT3信号通路的关系。方法:将胆囊癌细胞株GBC-SD用IL-6或IL-6+AG490(JAK/STAT3通路抑制剂)作用后,分别用MTT法检测增殖情况;Transwell法检测侵袭能力;明胶酶谱法检测基质金属蛋白酶9(MMP-9)活性;Western blot法检测磷酸化STAT3(p-STAT3)和血管内皮生长因子(VEGF)蛋白的表达。结果:IL-6(10,50,100 ng/mL)作用后,GBC-SD细胞增殖呈浓度依赖性增加(均P<0.05),AG490能取消IL-6对细胞增殖的促进作用。IL-6作用GBC-SD细胞后,细胞侵袭能力及MMP-9的分泌明显增加(均P<0.05),细胞p-STAT3和VEGF的表达明显上调,加入AG490后,以上作用均被取消。结论:IL-6能促进胆囊癌细胞的增殖通和侵袭,其作用可能与其活化JAK/STAT3信号通路,从而上调下游的MMP-9和VEGF的表达有关。
Objective: To investigate the effect of interleukin-6 (IL-6), an inflammatory cytokine, on the biological behavior of gallbladder carcinoma cells and its relationship with JAK / STAT3 signaling pathway. Methods: The proliferation of gallbladder carcinoma cell line GBC-SD was induced by IL-6 or IL-6 + AG490 (inhibitor of JAK / STAT3 pathway), MTT assay was used to detect the proliferation. Transwell assay was used to detect the invasion ability. Gelatin zymography The activity of MMP-9 was detected by Western blot. The expressions of p-STAT3 and VEGF were detected by Western blot. Results: The proliferation of GBC-SD cells increased in a concentration-dependent manner (all P <0.05) after treatment with IL-6 (10,50,100 ng / mL). AG490 abolished the promotion of IL-6 on cell proliferation. After GBC-SD cells were treated with IL-6, cell invasion and secretion of MMP-9 were significantly increased (all P <0.05), and the expression of p-STAT3 and VEGF was significantly up-regulated in cells treated with IL-6. Conclusion: IL-6 can promote the proliferation and invasion of gallbladder carcinoma cells, which may be related to the activation of JAK / STAT3 signaling pathway and the up-regulation of MMP-9 and VEGF expression.