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目的通过检测 Met 蛋白在胆囊癌组织中的表达和肝细胞生长因子(HGF)对胆囊癌细胞系生长、运动侵袭能力的影响来探讨 SF/HGF-Met 通路在胆囊癌进展中的作用。方法免疫组织化学(En Vision 二步法)检测 Met 在胆囊癌组织中表达,以慢性胆囊炎、胆囊腺瘤和肝移植供体胆囊标本为对照。采用噻唑蓝(MTT)比色法以及体外运动、侵袭实验观察不同浓度梯度的HGF 和格尔德霉素(GA)对胆囊癌细胞生长和运动侵袭能力的影响。结果 Met 在胆囊癌组织中表达+7.14%(3/42),++52.38%(22/42),+++40.48%(17/42),正常胆囊上皮和良性疾病胆囊上皮中正常胆囊和良性疾病-9.52%(2/21),+66.67%(14/21),++19.05%(4/21),+++4.76(1/21),在肿瘤组织中表达较强(P<0.01)。本次实验所设定的浓度 HGF 对胆囊癌细胞系的生长促进作用不明显。运动侵袭试验中 HGF 对 GBC-SD 细胞迁移运动侵袭能力有诱导作用,并呈剂量依赖效应。GA 本身对胆囊癌细胞运动侵袭能力抑制作用不明显,但是可以抑制 HGF 对胆囊癌细胞运动侵袭能力的诱导作用,差异有统计意义。结论本研究提示了 Met 过度表达与胆囊癌发展的相关性,HGF-Met 通路的激活在胆囊癌进展过程中起了一定作用。GA 类药物有望成为抑制胆囊癌转移的有效药物。
Objective To explore the role of SF / HGF-Met pathway in the progression of gallbladder carcinomas by detecting the expression of Met protein in gallbladder carcinomas and the effect of hepatocyte growth factor (HGF) on the growth and motility of gallbladder carcinoma cell lines. Methods Immunohistochemistry (En Vision two-step method) was used to detect the expression of Met in gallbladder carcinoma tissues. Chronic cholecystitis, gallbladder adenoma and donor gallbladder specimens were used as control. The effects of HGF and geldanamycin (GA) with different concentration gradients on the growth and motility of gallbladder carcinoma cells were observed by MTT colorimetric assay and in vitro motility and invasion assay. Results The expression of Met in gallbladder cancer tissues was + 7.14% (3/42), ++ 52.38% (22/42), +++ 40.48% (17/42), normal gallbladder epithelium and normal gallbladder epithelium The benign diseases were significantly (P <0.01) positive in benign diseases (-9.52%, 66.67% (14/21), ++ 19.05% (4/21), +++ 4.76 (1/21) 0.01). The experiment set HGF concentration on the growth of gallbladder cancer cell lines had no significant effect. HGF can induce migration of GBC-SD cells in a kinetic invasion assay in a dose-dependent manner. GA itself has no obvious inhibitory effect on the motility of the gallbladder carcinoma cells, but it can inhibit the induced effect of HGF on the motility of the gallbladder carcinoma cells. The difference was statistically significant. Conclusion This study suggests that Met overexpression correlates with the development of gallbladder carcinomas. The activation of HGF-Met pathway plays a role in the progression of gallbladder carcinomas. GA drugs is expected to become an effective drug to inhibit the metastasis of gallbladder cancer.