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EGFL7 drives the evolution of resistance to EGFR inhibitors in lung cancer by activating NOTCH signaling
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EGFL7 drives the evolution of resistance to EGFR inhibitors in lung cancer by activating NOTCH signaling
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Journal Article
EGFL7 drives the evolution of resistance to EGFR inhibitors in lung cancer by activating NOTCH signaling
2022
Overview
Accumulating evidence supports evolutionary trait of drug resistance. Like resilience in other systems, most tumor cells experience drug-tolerant state before full resistance acquired. However, the underlying mechanism is still poorly understood. Here, we identify that EGF like domain multiple 7 (
EGFL7
) is a responsive gene to epidermal growth factor receptor (EGFR) kinase inhibition during a period when tumors are decimated. Moreover, our data reveal that the adaptive increase of EGFL7 during this process is controlled by the depression of nonsense-mediated mRNA decay (NMD) pathway. Upregulation of EGFL7 activates NOTCH signaling in lung cancer cells, which slows down the decrease of c-Myc caused by EGFR inhibition, thereby helping the survival of cancer cells. Our data, taken together, demonstrate that EGFL7 is a driver gene for resistance to EGFR kinase inhibition, and suggest that targeting EGFL7/NOTCH signaling may improve the clinical benefits of EGFR inhibitors in patients with
EGFR
mutant tumors.
Publisher
Nature Publishing Group UK,Springer Nature B.V,Nature Publishing Group
Subject
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/ 38/39
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/ Biomedical and Life Sciences
/ Drug Resistance, Neoplasm - genetics
/ EGF Family of Proteins - metabolism
/ Endothelial Growth Factors - genetics
/ Endothelial Growth Factors - metabolism
/ Epidermal growth factor receptors
/ Humans
/ Intercellular Signaling Peptides and Proteins - metabolism
/ Kinases
/ Lung Neoplasms - drug therapy
/ Medicine
/ Mutation
/ Nonsense-mediated mRNA decay
/ Protein Kinase Inhibitors - pharmacology
/ Protein Kinase Inhibitors - therapeutic use
/ Transcription Factors - metabolism
/ Tumors
