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U. K. Misra, M. Gonzalez-Gronow, G. Gawdi, J. P. Johnson and S. V. Pizzo, “The Role of GRP78 in Alpha-2-Macroglobulin-Induced Signal Transduction. Evidence from RNA Interference That the Low Density Lipoprotein Receptor Related Protein Is Associaetd with but Not Necessary for GRP78-Mediated Signal Transformation,” The Journal of Biological Chemistry, Vol. 277, No. 44, 2002, pp. 42082-42087. doi:10.1074/jbc.M206174200

has been cited by the following article:

• 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.