MEMO1, a new IRS1-interacting protein, induces epithelial-mesenchymal transition in mammary epithelial cells

A. V. Sorokin; J. Chen

doi:10.1038/onc.2012.327

MEMO1, a new IRS1-interacting protein, induces epithelial-mesenchymal transition in mammary epithelial cells

A. V. Sorokin, J. Chen

Experimental Radiation Oncology

Research output: Contribution to journal › Article › peer-review

56 Scopus citations

Abstract

MEMO1 (mediator of ErbB2-driven cell motility 1) regulates HER2-dependent cell migration. Increased MEMO1 expression is associated with cancer aggressiveness. Here, we found that MEMO1 is also involved in breast carcinogenesis via regulating insulin-like growth factor-I receptor-dependent signaling events. We showed that MEMO1 binds to insulin receptor substrate 1, activates the downstream PI3K/Akt signaling pathway, leads to upregulation of Snail1 and thereby triggers the epithelial-mesenchymal transition (EMT) program. In addition, MEMO1 overexpression is accompanied by growth factor-independent proliferation, anchorage-independent growth in soft agar, and enhanced metastatic potential. Together, these findings suggest that MEMO1 acts as an oncogene and is a potential therapeutic target for cancer treatment.

Original language	English (US)
Pages (from-to)	3130-3138
Number of pages	9
Journal	Oncogene
Volume	32
Issue number	26
DOIs	https://doi.org/10.1038/onc.2012.327
State	Published - Jun 27 2013

Keywords

EMT
IRS1
MEMO1
Snail1
breast cancer

ASJC Scopus subject areas

Molecular Biology
Genetics
Cancer Research

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10.1038/onc.2012.327

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title = "MEMO1, a new IRS1-interacting protein, induces epithelial-mesenchymal transition in mammary epithelial cells",

abstract = "MEMO1 (mediator of ErbB2-driven cell motility 1) regulates HER2-dependent cell migration. Increased MEMO1 expression is associated with cancer aggressiveness. Here, we found that MEMO1 is also involved in breast carcinogenesis via regulating insulin-like growth factor-I receptor-dependent signaling events. We showed that MEMO1 binds to insulin receptor substrate 1, activates the downstream PI3K/Akt signaling pathway, leads to upregulation of Snail1 and thereby triggers the epithelial-mesenchymal transition (EMT) program. In addition, MEMO1 overexpression is accompanied by growth factor-independent proliferation, anchorage-independent growth in soft agar, and enhanced metastatic potential. Together, these findings suggest that MEMO1 acts as an oncogene and is a potential therapeutic target for cancer treatment.",

keywords = "EMT, IRS1, MEMO1, Snail1, breast cancer",

author = "Sorokin, {A. V.} and J. Chen",

note = "Funding Information: We thank all our colleagues in the Chen laboratory for insightful discussions and technical assistance. We thank Dr Douglas Yee at the University of Minnesota for sharing hIRS2 cDNA and Dr Cosima Baldari at the University of Siena (Italy) for sharing ShcA(p66) cDNA. This work was supported in part by an Era of Hope Research award to JC (W81XWH-09-1-0409). JC is also a recipient of an Era of Hope Scholar award from the Department of Defense (W81XWH-05-1-0470). This work was supported by MD Anderson{\textquoteright}s Cancer Center Support Grant (CA016672).",

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doi = "10.1038/onc.2012.327",

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N1 - Funding Information: We thank all our colleagues in the Chen laboratory for insightful discussions and technical assistance. We thank Dr Douglas Yee at the University of Minnesota for sharing hIRS2 cDNA and Dr Cosima Baldari at the University of Siena (Italy) for sharing ShcA(p66) cDNA. This work was supported in part by an Era of Hope Research award to JC (W81XWH-09-1-0409). JC is also a recipient of an Era of Hope Scholar award from the Department of Defense (W81XWH-05-1-0470). This work was supported by MD Anderson’s Cancer Center Support Grant (CA016672).

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N2 - MEMO1 (mediator of ErbB2-driven cell motility 1) regulates HER2-dependent cell migration. Increased MEMO1 expression is associated with cancer aggressiveness. Here, we found that MEMO1 is also involved in breast carcinogenesis via regulating insulin-like growth factor-I receptor-dependent signaling events. We showed that MEMO1 binds to insulin receptor substrate 1, activates the downstream PI3K/Akt signaling pathway, leads to upregulation of Snail1 and thereby triggers the epithelial-mesenchymal transition (EMT) program. In addition, MEMO1 overexpression is accompanied by growth factor-independent proliferation, anchorage-independent growth in soft agar, and enhanced metastatic potential. Together, these findings suggest that MEMO1 acts as an oncogene and is a potential therapeutic target for cancer treatment.

AB - MEMO1 (mediator of ErbB2-driven cell motility 1) regulates HER2-dependent cell migration. Increased MEMO1 expression is associated with cancer aggressiveness. Here, we found that MEMO1 is also involved in breast carcinogenesis via regulating insulin-like growth factor-I receptor-dependent signaling events. We showed that MEMO1 binds to insulin receptor substrate 1, activates the downstream PI3K/Akt signaling pathway, leads to upregulation of Snail1 and thereby triggers the epithelial-mesenchymal transition (EMT) program. In addition, MEMO1 overexpression is accompanied by growth factor-independent proliferation, anchorage-independent growth in soft agar, and enhanced metastatic potential. Together, these findings suggest that MEMO1 acts as an oncogene and is a potential therapeutic target for cancer treatment.

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KW - MEMO1

KW - Snail1

KW - breast cancer

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MEMO1, a new IRS1-interacting protein, induces epithelial-mesenchymal transition in mammary epithelial cells

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Keywords

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