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High expression of ErbB2 contributes to cholangiocarcinoma cell invasion and proliferation through AKT/p70S6K

World Journal of Gastroenterology 2010年第32期16卷 4047-4054页

作者： warapen treekitkarnmongkol Tuangporn Suthiphongchai Department of Biochemistry Faculty of ScienceMahidol UniversityBangkok 10400Thailand

AIM:To compare the impact of ErbB2 on cell invasion and proliferation in cholangiocarcinoma(CCA) cell ***:Level of endogenous ErbB2 expression in three CCA cell lines,namely HuCCA-1,KKU-100 and KKU-M213,was determined by real-time reversetranscriptase polymerase chain *** ErbB2 inhibitory methods,a small molecule ErbB2 kinase inhibitor(AG825) and siRNA,were used to disrupt ErbB2 function in the cell *** cell invasion,motility and proliferation under ErbB2-disrupted conditions were detected using Transwell and 3-(4,5-dimethylthiazol-2-yl)2,5-diphenyltetrazolium bromide *** addition,ErbB2 downstream effectors were investigated by Western blotting ***:Suppression of ErbB2 activity,using a specific kinase inhibitor(AG825),reduced invasion,motility and proliferation of all three CCA cell *** ability of this drug to inhibit neoplastic properties(invasion,motility and proliferation) increased concomitantly with the level of ErbB2 ***,knockdown of ErbB2 level by siRNA inhibited cell invasion and proliferation of KKU-M213,a high-ErbB2-expressing cell,better than those of the lower-ErbB2-expressing cells,HuCCA-1 and ***,both inhibitory methods indicated that there is more ErbB2-dependency for malignancy of the high-ErbB2-expressing cell,KKU-M213,than for that of low-ErbB2-expressing *** addition,interrupting ErbB2 activity decreased phosphorylation of AKT and p70S6K,but not extracellular signal-regulated kinase 1/2,in the high-ErbB2-expressing CCA cell ***:Our data indicated that high ErbB2 expression enhances CCA invasion,motility and proliferation via the AKT/p70S6K pathway,which suggests the possibility of targeting these molecules for CCA therapy.

关键词： AKT Cholangiocarcinoma ErbB2 Invasion p70S6K Cell proliferation

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