【摘 要】
：
The epithelial-mesenchymal transition(EMT)has been demonstrated to be a dominant program in colorectal cancer(CRC).It remains unclear how STC2 protein regulates EMT process and CRC development.In our
【机 构】
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State Key Laboratory of Biotherapy and Cancer Center,West China Hospital,Sichuan University/National
【出 处】
：
中国生物化学与分子生物学会2016年全国学术会议
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The epithelial-mesenchymal transition(EMT)has been demonstrated to be a dominant program in colorectal cancer(CRC).It remains unclear how STC2 protein regulates EMT process and CRC development.In our study,we found that the secretion and expression level of STC2 was both greatly increased in EMT cells and CRC cells compared with the normal epithelial NCM460 cells.And the conditional media from EMT cells induced epithelia and CRC cells to obtain EMT characterization.STC2 overexpression promoted CRC cell growth and cell migration,conversely STC2 knockdown inhibited cell migration and invasion.Besides EMT marker expression changes,several critical signaling pathway molecules including pERK,pAKT,PI3K and Ras were remarkably increased both in STC2-overexpressing NCM460 cells and in cells incubated with exogenous STC2 proteins.However several key EMT markers were changed when blocking AKT-ERK signaling pathways.Moreover the elevated STC2 in CRC tumors and high serum STC2 level are associated with tumor pathologic stage and poor survival for CRC.Our data indicate STC2 promotes CRC tumorigenesis and EMT progression process through regulating ERK/MEK and PI3K/AKT signaling pathways.
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