摘要
目的探讨奥曲肽对转化生长因子α(TGF-α)诱导肝癌细胞增殖的抑制作用及其机制。方法用免疫组化法观察奥曲肽对TGF-α诱导肝癌细胞增殖的影响,用逆转录-聚合酶链反应(RT-PCR)检测奥曲肽对肝癌细胞TGF-α分泌和表皮生长因子受体(EGFR)表达的影响,用Western-blot法、免疫组化法检测奥曲肽对细胞外信号调节蛋白激酶(ERK)的影响。结果奥曲肽明显抑制细胞核内TGF-α诱导的增殖细胞核抗原(PCNA)表达,使肝癌细胞TGF-αmRNA指数较对照组降低(P<0.05),对TGF-α诱导的EGFRmRNA指数的增加具有明显抑制作用。Western-blot显示,奥曲肽明显抑制TGF-α诱导的ERK蛋白表达;免疫组化显示,TGF-α作用后,胞核染色明显加深,奥曲肽与TGF-α同时作用后胞核染色明显减弱。结论奥曲肽可能通过抑制肝癌细胞分泌TGF-α,抑制EGFR表达和阻断EGFR信号传导,从而抑制TGF-α诱导的肝癌细胞增殖。
Objective To investigate the inhibitory effect of octreotide on transforming growth factor-alpha （TGF-α）-induced cell proliferation of human hepatocellular carcinoma cells and its possible mechanism. Methods The effect of octreotide on TGF-α-induced cell proliferation of the liver cancer cells （ LCC ） was evaluated by immunohistochemistry method. The effect of octreotide on TGF-α secretion and epidermal growth factor receptor （EGFR） expression in the cells was determined by reverse-transcriptase polymerase chain reaction（RT-PCR）. The effect of octreotide on extracellular sigual-regulated protein kinase （ ERK ） expression in the cells was measured by Western-blot and immunohistochemistry method. Results The TGF-α-induced expressions of proliferating cell nuclear antigen （PCNA） in nucleus were obviously increased by TGF-α. TGF-αmRNA index of hepatocellular carcinoma cells was decreased by octreotide. Octreotide inhibited significantly the expressions of EGFR mRNA induced by TGF-α. Octreotide inhibited siguificanfly the expressions of ERK protein induced by TGF-α. There was intense staining in the nucleus of the cells by TGF-α and weak＇ staining in the nucleus of the cells treated simultaneously by octreotide and TGF-α. Conclusions Octreotide can inhibit the secretion of TGF-α, the expression of EGFR, and the signal transduction of EGFR of LCC, and consequently exerts an inhibitory effect on TGF-α-induced hepatocellular carcinoma cells proliferation.
出处
《中国普通外科杂志》
CAS
CSCD
2007年第3期218-222,共5页
China Journal of General Surgery
关键词
肝肿瘤
奥曲肽/治疗应用
转化生长因子Α
信号传导
Liver Neoplasms
Octreotide/ther use
Transforming Growth Factor-alpha
Singal Transduction
