Cited by 434

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Genetic Dissection of the Oncogenic mTOR Pathway Reveals Druggable Addiction to Translational Control via 4EBP-eIF4E

Hsieh, Andrew C., Costa, Maria, Zollo, Ornella, Davis, Cole, Feldman, Morris E., Testa, Joseph R., Meyuhas, Oded, Shokat, Kevan M., Ruggero, Davide·2010·Cancer Cell

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Crossref · 10.1016/j.ccr.2010.01.021

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  • TORC1 inhibition, via loss of 4EBP1 phosphorylation, results in a decrease of MCL-1 protein expression in some cancers.

    “TORC1 inhibition, via loss of 4EBP1 (also referred to as EIF4EBP1) phosphorylation, results in a decrease of MCL-1 protein expression in these cancers (37–40).”

    From mTOR Inhibition Specifically Sensitizes Colorectal Cancers with KRAS or BRAF Mutations to BCL-2/BCL-XL Inhibition by Suppressing MCL-1 (2014) · cites this paper as [37]

    The Results section on T-cell progenitor survival reports that Mcl-1 protein is elevated in AKTT thymocytes and returns to normal when a phosphorylation-defective 4EBP1 mutant restrains eIF4E activity. This supports the proposed 4EBP1–eIF4E–Mcl-1 link, but the Mcl-1 measurement is in thymocytes; it does not directly establish that TORC1 inhibition decreases MCL-1 protein in the cancers referenced by the citing sentence. (LLM, conf=0.86)

    Experimental — accuracy not yet measured
  • Efficient translation of MCL-1 mRNA requires cap-dependent translation in some cancers.

    “Previous studies had demonstrated that efficient translation of MCL-1 mRNA requires cap-dependent translation in some cancers (36–38).”

    From mTOR Inhibition Specifically Sensitizes Colorectal Cancers with KRAS or BRAF Mutations to BCL-2/BCL-XL Inhibition by Suppressing MCL-1 (2014) · cites this paper as [37]

    The Results section on Mcl-1 reports that its protein level, but not its mRNA level, rises in AKTT mouse thymocytes and that the increase depends on eIF4E activity. The paper also links oncogenic Akt to increased cap-dependent translation. It does not directly establish that efficient translation of MCL-1 mRNA requires cap-dependent translation in cancer cells; the Mcl-1 experiments described here concern thymocytes before tumor formation. (LLM, conf=0.82)

    Experimental — accuracy not yet measured

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Citations

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Research works printed but not linked: 45

  1. Alliouachene, 2008, Constitutively active Akt1 expression in mouse pancreas requires S6 kinase 1 for insulinoma formation, J. Clin. Invest., 118, 3629, 10.1172/JCI35237 · DOI
  2. Avdulov, 2004, Activation of translation complex eIF4F is essential for the genesis and maintenance of the malignant phenotype in human mammary epithelial cells, Cancer Cell, 5, 553, 10.1016/j.ccr.2004.05.024 · DOI
  3. Barna, 2008, Suppression of Myc oncogenic activity by ribosomal protein haploinsufficiency, Nature, 456, 971, 10.1038/nature07449 · DOI
  4. Brunn, 1997, Phosphorylation of the translational repressor PHAS-I by the mammalian target of rapamycin, Science, 277, 99, 10.1126/science.277.5322.99 · DOI · Paper page
  5. Buckland, 2000, Co-ordination of the expression of the protein tyrosine kinase p56(lck) with the pre-T cell receptor during thymocyte development, Eur. J. Immunol., 30, 8, 10.1002/1521-4141(200001)30:1<8::AID-IMMU8>3.0.CO;2-8 · DOI
  6. Choo, 2008, Rapamycin differentially inhibits S6Ks and 4E-BP1 to mediate cell-type-specific repression of mRNA translation, Proc. Natl. Acad. Sci. USA, 105, 17414, 10.1073/pnas.0809136105 · DOI
  7. Ciofani, 2006, A survival guide to early T cell development, Immunol. Res., 34, 117, 10.1385/IR:34:2:117 · DOI
  8. Feldman, 2009, Active-site inhibitors of mTOR target rapamycin-resistant outputs of mTORC1 and mTORC2, PLoS Biol., 7, e38, 10.1371/journal.pbio.1000038 · DOI
  9. Gingras, 1998, 4E-BP1, a repressor of mRNA translation, is phosphorylated and inactivated by the Akt(PKB) signaling pathway, Genes Dev., 12, 502, 10.1101/gad.12.4.502 · DOI
  10. Gingras, 1999, Regulation of 4E-BP1 phosphorylation: a novel two-step mechanism, Genes Dev., 13, 1422, 10.1101/gad.13.11.1422 · DOI
  11. Gingras, 1999, eIF4 initiation factors: effectors of mRNA recruitment to ribosomes and regulators of translation, Annu. Rev. Biochem., 68, 913, 10.1146/annurev.biochem.68.1.913 · DOI
  12. Guertin, 2007, Defining the role of mTOR in cancer, Cancer Cell, 12, 9, 10.1016/j.ccr.2007.05.008 · DOI · Paper page
  13. Guertin, 2009, The pharmacology of mTOR inhibition, Sci. Signal., 2, pe24, 10.1126/scisignal.267pe24 · DOI
  14. Haghighat, 1997, eIF4G dramatically enhances the binding of eIF4E to the mRNA 5′-cap structure, J. Biol. Chem., 272, 21677, 10.1074/jbc.272.35.21677 · DOI
  15. Hay, 2004, Upstream and downstream of mTOR, Genes Dev., 18, 1926, 10.1101/gad.1212704 · DOI · Paper page
  16. Juntilla, 2007, Akt1 and Akt2 are required for alphabeta thymocyte survival and differentiation, Proc. Natl. Acad. Sci. USA, 104, 12105, 10.1073/pnas.0705285104 · DOI
  17. Kim, 2002, mTOR interacts with raptor to form a nutrient-sensitive complex that signals to the cell growth machinery, Cell, 110, 163, 10.1016/S0092-8674(02)00808-5 · DOI
  18. Kozma, 1990, Cloning of the mitogen-activated S6 kinase from rat liver reveals an enzyme of the second messenger subfamily, Proc. Natl. Acad. Sci. USA, 87, 7365, 10.1073/pnas.87.19.7365 · DOI
  19. Labrecque, 2001, How much TCR does a T cell need?, Immunity, 15, 71, 10.1016/S1074-7613(01)00170-4 · DOI
  20. Lambertsson, 1998, The minute genes in Drosophila and their molecular functions, Adv. Genet., 38, 69, 10.1016/S0065-2660(08)60142-X · DOI
  21. Leenders, 2000, Role of the forkhead transcription family member, FKHR, in thymocyte differentiation, Eur. J. Immunol., 30, 2980, 10.1002/1521-4141(200010)30:10<2980::AID-IMMU2980>3.0.CO;2-9 · DOI
  22. Malstrom, 2001, Tumor induction by an Lck-MyrAkt transgene is delayed by mechanisms controlling the size of the thymus, Proc. Natl. Acad. Sci. USA, 98, 14967, 10.1073/pnas.231467698 · DOI
  23. Mao, 2007, Unequal contribution of Akt isoforms in the double-negative to double-positive thymocyte transition, J. Immunol., 178, 5443, 10.4049/jimmunol.178.9.5443 · DOI
  24. Mende, 2001, Oncogenic transformation induced by membrane-targeted Akt2 and Akt3, Oncogene, 20, 4419, 10.1038/sj.onc.1204486 · DOI
  25. Mothe-Satney, 2000, Multiple mechanisms control phosphorylation of PHAS-I in five (S/T)P sites that govern translational repression, Mol. Cell. Biol., 20, 3558, 10.1128/MCB.20.10.3558-3567.2000 · DOI
  26. Oliver, 2004, Ribosomal protein L24 defect in belly spot and tail (Bst), a mouse Minute, Development, 131, 3907, 10.1242/dev.01268 · DOI · Paper page
  27. Opferman, 2003, Development and maintenance of B and T lymphocytes requires antiapoptotic MCL-1, Nature, 426, 671, 10.1038/nature02067 · DOI
  28. Rajasekhar, 2003, Oncogenic Ras and Akt signaling contribute to glioblastoma formation by differential recruitment of existing mRNAs to polysomes, Mol. Cell, 12, 889, 10.1016/S1097-2765(03)00395-2 · DOI · Paper page
  29. Ruggero, 2005, The Akt of translational control, Oncogene, 24, 7426, 10.1038/sj.onc.1209098 · DOI
  30. Ruggero, 2004, The translation factor eIF-4E promotes tumor formation and cooperates with c-Myc in lymphomagenesis, Nat. Med., 10, 484, 10.1038/nm1042 · DOI
  31. Ruvinsky, 2006, Ribosomal protein S6 phosphorylation: from protein synthesis to cell size, Trends Biochem. Sci., 31, 342, 10.1016/j.tibs.2006.04.003 · DOI
  32. Ruvinsky, 2005, Ribosomal protein S6 phosphorylation is a determinant of cell size and glucose homeostasis, Genes Dev., 19, 2199, 10.1101/gad.351605 · DOI
  33. Schmitt, 2002, Induction of T cell development from hematopoietic progenitor cells by delta-like-1 in vitro, Immunity, 17, 749, 10.1016/S1074-7613(02)00474-0 · DOI · Paper page
  34. Schultz, 1929, The minute reaction in the development of Drosophila melanogaster, Genetics, 14, 366, 10.1093/genetics/14.4.366 · DOI
  35. Shortman, 1996, Early T lymphocyte progenitors, Annu. Rev. Immunol., 14, 29, 10.1146/annurev.immunol.14.1.29 · DOI
  36. Skeen, 2006, Akt deficiency impairs normal cell proliferation and suppresses oncogenesis in a p53-independent and mTORC1-dependent manner, Cancer Cell, 10, 269, 10.1016/j.ccr.2006.08.022 · DOI
  37. Staal, 1987, Molecular cloning of the akt oncogene and its human homologues AKT1 and AKT2: amplification of AKT1 in a primary human gastric adenocarcinoma, Proc. Natl. Acad. Sci. USA, 84, 5034, 10.1073/pnas.84.14.5034 · DOI
  38. Stolovich, 2002, Transduction of growth or mitogenic signals into translational activation of TOP mRNAs is fully reliant on the phosphatidylinositol 3-kinase-mediated pathway but requires neither S6K1 nor rpS6 phosphorylation, Mol. Cell. Biol., 22, 8101, 10.1128/MCB.22.23.8101-8113.2002 · DOI
  39. Tan, 2008, A novel recurrent chromosomal inversion implicates the homeobox gene Dlx5 in T-cell lymphomas from Lck-Akt2 transgenic mice, Cancer Res., 68, 1296, 10.1158/0008-5472.CAN-07-3218 · DOI
  40. Tang, 2001, Amino acid-induced translation of TOP mRNAs is fully dependent on phosphatidylinositol 3-kinase-mediated signaling, is partially inhibited by rapamycin, and is independent of S6K1 and rpS6 phosphorylation, Mol. Cell. Biol., 21, 8671, 10.1128/MCB.21.24.8671-8683.2001 · DOI
  41. von Manteuffel, 1997, The insulin-induced signalling pathway leading to S6 and initiation factor 4E binding protein 1 phosphorylation bifurcates at a rapamycin-sensitive point immediately upstream of p70s6k, Mol. Cell. Biol., 17, 5426, 10.1128/MCB.17.9.5426 · DOI
  42. Wendel, 2004, Survival signalling by Akt and eIF4E in oncogenesis and cancer therapy, Nature, 428, 332, 10.1038/nature02369 · DOI
  43. Yoon, 2006, Impaired control of IRES-mediated translation in X-linked dyskeratosis congenita, Science, 312, 902, 10.1126/science.1123835 · DOI
  44. Yuan, 2008, PI3K pathway alterations in cancer: variations on a theme, Oncogene, 27, 5497, 10.1038/onc.2008.245 · DOI · Paper page
  45. Zuniga-Pflucker, 2004, T-cell development made simple, Nat. Rev. Immunol., 4, 67, 10.1038/nri1257 · DOI

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Metadata

Authors
Hsieh, A. C., Costa, M., Zollo, O., Davis, C., Feldman, M. E., Testa, J. R., Meyuhas, O., Shokat, K. M., & Ruggero, D.
Venue
Cancer Cell
Publisher
Elsevier BV
Published
2010-03
Volume
17
Issue
3
Pages
249-261
ISSN
1535-6108
Cited by
434
References
4
Language
en

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