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V. Facchinetti, W. Ouyang, H. Wei, N. Soto, A. Lazorchak, C. Gould, C. Lowry, A. C. Newton, Y. Mao, R. Q. Miao, W. C. Sessa, J. Qin, P. Zhang, B. Su and E. Jacinto, “The Mammalian Targeted Rapamycin Complex 2 Targeted Rapamycin Complex-2 Controls Folding and Stability of Akt and Protein Kinase C,” EMBO Journal, Vol. 27, No. 14, 2008, pp. 1932-1943. doi:10.1038/emboj.2008.120

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• TITLE: iTorin1—An Active Site Inhibitor of mTOR, Suppresses Prostate Cancer Cell Growth Induced by Activated α2M-Macroglobulin Ligation of Cell Surface GRP78

  AUTHORS: Uma K. Misra, Salvatore V. Pizzo

  KEYWORDS: α2-Macroglobulin; Torin1; Prostate Cancer Cells Proliferation; p-S6KT389; p-4EBP1; p-AktS473; Insulin

  JOURNAL NAME: Journal of Cancer Therapy, Vol.4 No.4A, April 30, 2013

  ABSTRACT: In this study, we reported the effect of the ATP binding site competitive inhibitor Torin1 on activated α2-macroglobulin (α2M*)-induced cell proliferation and activation of mTORC1 and mTORC2 signaling in prostate cancer cells. Torin1 significantly inhibited α2M*-induced cellproliferation as measured by protein and DNA synthesis. Translational activity, a major cellular response in malignant cells,is coordinately regulated by the mTORC1-S6-kinaseand mTORC1-4EBP1 axes. Torin1 significantly inhibited α2M*- and insulin-induced activation of mTORC1 as determined by phosphorylation of S6-kinaseat Thr389 and 4EBP1 at Thr37/46 compared to untreated cells employing Raptor immunoprecipitates. Torin1 also significantly inhibited α2M*- and insulin-induced upregulation of p-AktT308 and p-AktS473 in prostate cancer cells. The effect was comparable to that of insulin employed as a positive control. Finally, Torin1 inhibited α2M*- and insulin-induced activation of mTORC2 kinase assayas measured by phosphorylation of Akt at Ser473 inRictor immunoprecipitates of prostate cancer cells.