Functional Redundancy between β1 and β3 Integrin in Activating the IR/Akt/mTORC1 Signaling Axis to Promote ErbB2-Driven Breast Cancer-Reference-Cited by-同舟云学术

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Functional Redundancy between β1 and β3 Integrin in Activating the IR/Akt/mTORC1 Signaling Axis to Promote ErbB2-Driven Breast Cancer

Published:2019-10 Issue:3 Volume:29 Page:589-602.e6
ISSN:2211-1247
Container-title:Cell Reports
language:en
Short-container-title:Cell Reports

Author:

Bui Tung,Rennhack Jonathan,Mok Stephanie,Ling Chen,Perez Marco,Roccamo Joshua,Andrechek Eran R.,Moraes Christopher,Muller William J.

Funder

Canadian Institutes of Health Research Foundation

Cedars Cancer Institute

McGill Integrated Cancer Research Training Program

Natural Sciences and Engineering Research Council

Canada Research Chair in Advanced Cellular Microenvironments

Canada Research Chair in Molecular Oncology

Publisher

Elsevier BV

Subject

General Biochemistry, Genetics and Molecular Biology

Reference52 articles.

1. Human breast cancer invasion and aggression correlates with ECM stiffening and immune cell infiltration;Acerbi;Integr. Biol.,2015

2. Amplification of the neu/erbB-2 oncogene in a mouse model of mammary tumorigenesis;Andrechek;Proc. Natl. Acad. Sci. USA,2000

3. neu/erbB-2 amplification identifies a poor-prognosis group of women with node-negative breast cancer;Andrulis;J. Clin. Oncol.,1998

4. Linking integrin conformation to function;Askari;J. Cell Sci.,2009

5. Beta 1-integrin-c-Met cooperation reveals an inside-in survival signalling on autophagy-related endomembranes;Barrow-McGee;Nat. Commun.,2016

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