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p‐AKT regulates translocalization of snail in oral cancer
Author(s) -
Hong SeongDoo,
Hong KyoungOk,
Hong JiSoo,
Lee JaeIl,
Hong SamPyo
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.5.a387-d
Subject(s) - protein kinase b , snail , pi3k/akt/mtor pathway , cancer research , phosphorylation , gsk 3 , chemistry , kinase , epithelial–mesenchymal transition , cancer , microbiology and biotechnology , biology , signal transduction , medicine , metastasis , ecology
Epithelial‐mesenchymal transition (EMT) plays a pivotal role in the conversion of early stage tumors into invasive malignancies, and has been shown to be regulated by the transcriptional factor, Snail. Recently, activation of the phosphatidylinositol 3′ kinase (PI3K)/AKT axis is emerging as a central feature of EMT. However, it is unclear whether the phosphorylation of AKT regulate the expression of snail in oral cancer cell underwent EMT. To investigate a role of p‐AKT in EMT, we assessed the effects of inhibiting p‐AKT activity in oral squamous cancer cells (KOSCC‐25B) using PIAs, structurally modified phosphatidylinositol ether lipid analogues (PIAs). PIAs decreased phosphorylation of c‐Jun N‐terminal Kinase(JNK) and increased phosphorylation of glycogen synthase kinase 3beta (GSK‐3beta). Inhibition of p‐AKT induced down regulation of Snail and Twist, but Sip1 regulated independent of p‐AKT inhibition. Also inhibition of p‐AKT decreased cell migration and invasion. Therefore our results implicate that p‐AKT may contribute to the translocalization of snail in the EMT associated with cancer cell migration and invasion.