MiR-155 promotes epithelial-mesenchymal transition in hepatocellular carcinoma cells through the activation of PI3K/SGK3/β-catenin signaling pathways
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Xin Kong1, Fengchao Liu1, Jian Gao1
1Department of Gastroenterology, Second Affiliated Hospital, Chongqing Medical University, Chongqing, China
Jian Gao, email: firstname.lastname@example.org
Keywords: epithelial-mesenchymal transition, SGK3, miR-155, hepatocellular carcinoma, phosphatidylinositol-3-kinase
Received: March 01, 2016 Accepted: August 24, 2016 Published: September 01, 2016
Oncogenic mutations in PIK3CA, the gene encoding the catalytic subunit of phosphoinositide 3-kinase (PI3K), occur with high frequency in hepatocellular carcinoma (HCC). The protein kinase Akt is considered to be the primary effector of PI3K, but there is evidence to suggest that serum and glucocorticoid kinase 3 (SGK3) acts in an Akt-independent manner downstream of PI3K. In this report, we found that SGK3 promotes epithelial-mesenchymal transition (EMT) and reduces phosphorylation-dependent degradation of β-catenin in HCC cells. We determined that miR-155, previously shown to promote EMT, stimulates the expression of SGK3 by targeting and repressing P85α, thereby removing its inhibitory effect on PI3K-AKT signaling. These findings suggest that miR-155 promotes EMT and metastatic properties in HCC cells through activation of PI3K/SGK3/β-catenin signaling pathways.
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