Purpose It has been reported that PI3K/AKT pathway is altered in various cancers and AKT isoforms specifically regulate cell growth and metastasis of cancer cells; AKT1, but not AKT2, reduces invasion of cancer cells but maintains cancer /BTG2 growth. We propose here a novel mechanism of the tumor suppresser, TIS21 , that inhibits both growth and invasion of triple negative breast cancer cells via AKT1 activation by differential regulation of mTORc1 and mTORc2 activity. /BTG2 Methods Transduction of adenovirus carrying TIS21 gene and transfection of short interfering RNAs were employed /BTG2 to regulate TIS21 gene expression in various cell lines. Treatment of mTOR inhibitors and mTOR kinase assays can /BTG2 evaluate the role of mTORc in the regulation of AKT phosphorylation at S473 residue by TIS21 in breast cancer cells. /BTG2 Open data and immunohistochemical analysis were performed to confirm the role of TIS21 expression in various human breast cancer tissues. /BTG2 Results We observed that TIS21 inhibited mTORc1 activity by reducing Raptor-mTOR interaction along with upregu- S473 lation of tsc1 expression, which lead to significant reduction of p70S6K activation as opposed to AKT1 , but not AKT2, /BTG2 S473 phosphorylation via downregulating PHLPP2 (AKT1-specific phosphatase) in breast cancers.
Journal of Cancer Research and Clinical Oncology – Springer Journals
Published: May 28, 2018
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