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mTORC1 promotes survival through translational control of Mcl-1.

Abstract：

:Activation of the phosphatidylinositol 3-kinase (PI3K)/AKT signaling pathway is a frequent occurrence in human cancers and a major promoter of chemotherapeutic resistance. Inhibition of one downstream target in this pathway, mTORC1, has shown potential to improve chemosensitivity. However, the mechanisms and genetic modifications that confer sensitivity to mTORC1 inhibitors remain unclear. Here, we demonstrate that loss of TSC2 in the E mu-myc murine lymphoma model leads to mTORC1 activation and accelerated oncogenesis caused by a defective apoptotic program despite compromised AKT phosphorylation. Tumors from Tsc2(+/-)E mu-Myc mice underwent rapid apoptosis upon blockade of mTORC1 by rapamycin. We identified myeloid cell leukemia sequence 1 (Mcl-1), a bcl-2 like family member, as a translationally regulated genetic determinant of mTORC1-dependent survival. Our results indicate that the extent by which rapamycin can modulate expression of Mcl-1 is an important feature of the rapamycin response.

journal_name

Proc Natl Acad Sci U S A

journal_title

Proceedings of the National Academy of Sciences of the United States of America

authors

Mills JR,Hippo Y,Robert F,Chen SM,Malina A,Lin CJ,Trojahn U,Wendel HG,Charest A,Bronson RT,Kogan SC,Nadon R,Housman DE,Lowe SW,Pelletier J

doi

10.1073/pnas.0804821105

subject

Has Abstract

pub_date

2008-08-05 00:00:00

pages

10853-8

issue

31

eissn

0027-8424

issn

1091-6490

pii

0804821105

journal_volume

105

pub_type

杂志文章

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