Expression and function of the insulin receptor substrate proteins in cancer
Open accessAbstract
The Insulin Receptor Substrate (IRS) proteins are cytoplasmic adaptor proteins that function as essential signaling intermediates downstream of activated cell surface receptors, many of which have been implicated in cancer. The IRS proteins do not contain any intrinsic kinase activity, but rather serve as scaffolds to organize signaling complexes and initiate intracellular signaling pathways. As common intermediates of multiple receptors that can influence tumor progression, the IRS proteins are positioned to play a pivotal role in regulating the response of tumor cells to many different microenvironmental stimuli. Limited studies on IRS expression in human tumors and studies on IRS function in human tumor cell lines and in mouse models have provided clues to the potential function of these adaptor proteins in human cancer. A general theme arises from these studies; IRS-1 and IRS-4 are most often associated with tumor growth and proliferation and IRS-2 is most often associated with tumor motility and invasion. In this review, we discuss the mechanisms by which IRS expression and function are regulated and how the IRS proteins contribute to tumor initiation and progression.
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By phosphorylating adaptor proteins, most notably the insulin receptor substrate (IRS) family, the initial kinase event is linked to downstream signaling pathways.
“By phosphorylating adaptor proteins, most notably the insulin receptor substrate (IRS) family, the initial kinase event is linked to downstream signaling pathways (52).”
From Diabetes and Cancer (2010) · cites this paper as [52]
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References 183 · Cited by 192
- Authors
- Mardilovich, K., Pankratz, S. L., & Shaw, L. M.
- Affiliations
- University of Massachusetts Chan Medical School (US)
- Corresponding author
- Shaw, Leslie M
- Venue
- Cell Communication and Signaling
- Published
- 2009-06-17
- Volume
- 7
- Issue
- 1
- Pages
- 14-14
- ISSN
- 1478-811X (ISSN-L)
- PMC
- PMC2709114
- OpenAlex
- W2096913544
- Cited by
- 192
- References
- 183
- Citations by year
- 2026: 7 · 2025: 8 · 2024: 15 · 2023: 14 · 2022: 16 · 2021: 14 · 2020: 14 · 2019: 12 · 2018: 14 · 2017: 11 · 2016: 5 · 2015: 6 · 2014: 12 · 2013: 8 · 2012: 13
- FWCI
- 4.70
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- cc-by
- Locations
- Cell Communication and Signaling (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- eScholarship@UMassChan (submittedVersion, cc-by)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- U.S. Department of Defense
- National Institutes of Health
- National Cancer Institute (R01CA090583)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
- Keywords
- IRS-1, insulin receptor substrate 2, adaptor proteins, cancer signaling, tumor progression, tumor microenvironment, tumor initiation
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