simultaneous inhibition of mtor-containing complex 1 (mtorc1) and mnk induces apoptosis of cutaneous t-cell lymphoma (ctcl) cells同时抑制mtor-containing复杂1(mtorc1)和mnk皮肤t细胞淋巴瘤(ctcl)细胞的凋亡.pdfVIP
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simultaneous inhibition of mtor-containing complex 1 (mtorc1) and mnk induces apoptosis of cutaneous t-cell lymphoma (ctcl) cells同时抑制mtor-containing复杂1(mtorc1)和mnk皮肤t细胞淋巴瘤(ctcl)细胞的凋亡
Simultaneous Inhibition of mTOR-Containing Complex 1
(mTORC1) and MNK Induces Apoptosis of Cutaneous T-
Cell Lymphoma (CTCL) Cells
1 1 2 2 3 1
Michal Marzec , Xiaobin Liu , Maria Wysocka , Alain H. Rook , Niels Odum , Mariusz A. Wasik *
1 Department of Pathology and Laboratory Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, United States of America, 2 Department of Dermatology,
University of Pennsylvania, Philadelphia, Pennsylvania, United States of America, 3 Institute of Molecular Biology, University of Copenhagen, Copenhagen, Denmark
Abstract
Background: mTOR kinase forms the mTORC1 complex by associating with raptor and other proteins and affects a number
of key cell functions. mTORC1 activates p70S6kinase 1 (p70S6K1) and inhibits 4E-binding protein 1 (4E-BP1). In turn,
p70S6K1 phosphorylates a S6 protein of the 40S ribosomal subunit (S6rp) and 4E-BP1, with the latter negatively regulating
eukaryotic initiation factor 4E (eIF-4E). MNK1 and MNK2 kinases phosphorylate and augment activity of eIF4E. Rapamycin
and its analogs are highly specific, potent, and relatively non-toxic inhibitors of mTORC1. Although mTORC1 activation is
present in many types of malignancies, rapamycin-type inhibitors shows relatively limited clinical efficacy as single agents.
Initially usually indolent, CTCL displays a tendency to progress to the aggressive forms with limited response to therapy and
poor prognosis. Our previous study (M. Marzec et al. 2008) has demonstrated that CTCL cells display mTORC1 activation and
short-term treatment of CTCL-derived cells with rapamycin suppressed their proliferation and had little effect on the cell
survival.
Methods: Cells derived from CTCL were treated with mTORC1 inhibitor rapamycin and MNK inhi
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