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Integrin-mediated resistance to epidermal growth factor receptor-targeted therapy: an inflammatory situation
Journal article   Open access   Peer reviewed

Integrin-mediated resistance to epidermal growth factor receptor-targeted therapy: an inflammatory situation

Wells S Brown and Michael K Wendt
Breast cancer research : BCR, Vol.16(5), pp.1-3
09/23/2014
DOI: 10.1186/s13058-014-0448-0
PMCID: PMC4728772
PMID: 25255930
url
https://doi.org/10.1186/s13058-014-0448-0View
Published (Version of record) Open Access

Abstract

Targeting the function of epidermal growth factor receptor (EGFR) has failed as an effective clinical option for breast cancer. Understanding the drivers of inherent resistance has been a challenge. One possible mechanism is the acquisition of stem-like properties through the process of epithelial-mesenchymal transition. A recent study by Seguin and colleagues adds to our understanding of this process by demonstrating a functional role for unligated αvβ3 integrin in mediating a stem-like phenotype and facilitating resistance to EGFR-targeted therapy via enhanced downstream coupling to a KRAS:RalB:NF-κB pathway. Importantly, the identified mechanism may reveal a possible strategy for sensitizing breast cancer cells to EGFR-targeted therapies.
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