Phosphatase of regenerating liver 3(PRL3)promotes colorectal cancer(CRC)metastasis by inducing epithelial-to-mesenchymal transition.Mesenchymal-to-epithelial transition(MET),the opposite of epithelial-to-mesenchymal t...Phosphatase of regenerating liver 3(PRL3)promotes colorectal cancer(CRC)metastasis by inducing epithelial-to-mesenchymal transition.Mesenchymal-to-epithelial transition(MET),the opposite of epithelial-to-mesenchymal transition,has been proposed as a mechanism for the establishment of metastatic neoplasms.However,the molecular mechanism of MET remains unclear.Here,we show that miR-203a-3p derived from hepatocyte exosomes inhibits Src expression,reduces epidermal growth factor receptor activity and downstream signaling pathways,and increases E-cadherin expression,which is a typical mesenchymal cell marker of MET,in CRC cells.These results show the important role of epidermal growth factor receptor in CRC cell MET.展开更多
基金This work was supported by Grant from Key Laboratory of Malignant Tumor Molecular Mechanism and Translational Medicine of Guangzhou Bureau of Science and Information TechnologyGrant from the Key Laboratory of Malignant Tumor Gene Regulation and Target Therapy of Guangdong Higher Education Institutes+3 种基金and financially supported by the grants from National Natural Science Foundation of China(nos.81602539,81702902,81602125)Natural Science Foundation of Guangdong Province(no.2016A030310183)International Science and Technology Cooperation Program of Guangdong Province(no.2015A050502021)Science and Technology of Guangdong Province(no.201400000004-5).
文摘Phosphatase of regenerating liver 3(PRL3)promotes colorectal cancer(CRC)metastasis by inducing epithelial-to-mesenchymal transition.Mesenchymal-to-epithelial transition(MET),the opposite of epithelial-to-mesenchymal transition,has been proposed as a mechanism for the establishment of metastatic neoplasms.However,the molecular mechanism of MET remains unclear.Here,we show that miR-203a-3p derived from hepatocyte exosomes inhibits Src expression,reduces epidermal growth factor receptor activity and downstream signaling pathways,and increases E-cadherin expression,which is a typical mesenchymal cell marker of MET,in CRC cells.These results show the important role of epidermal growth factor receptor in CRC cell MET.
