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NF-κB-driven improvement of EHD1 contributes to erlotinib resistance in EGFR-mutant lung cancers

Wang, Xiaoyuan, Yin, Hang, Zhang, Hongxia, Hu, Jing, Lu, Hailing, Li, Chunhong, Cao, Mengru, Yan, Shi, Cai, Li·2018·Cell Death & Disease
DOI 10.1038/s41419-018-0447-7PMC PMC5856828
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Abstract

Acquired resistance to epidermal growth factor receptor-tyrosine-kinase inhibitors (EGFR-TKIs), such as gefitinib and erlotinib, is a critical obstacle in the treatment of EGFR mutant-positive non-small cell lung cancer (NSCLC). EHD1, a protein of the C-terminal Eps15 homology domain-containing (EHD) family, plays a role in regulating endocytic recycling, but the mechanistic details involved in EGFR-TKI resistance and cancer stemness remain largely unclear. Here, we found that a lower EHD1 expression improved both EGFR-TKIs sensitivity, which is consistent with a lower CD133 expression, and progression-free survival in NSCLC patients. The overexpression of EHD1 markedly increased erlotinib resistance and lung cancer cell stemness in vitro and in vivo. Moreover, we demonstrated that miR-590 targeted the 3′-UTR of EHD1 and was regulated by NK-κB, resulting in downregulated EHD1 expression, increased erlotinib sensitivity and repressed NSCLC cancer stem-like properties in vitro and in vivo. We found that EHD1 was an important factor in EGFR-TKI resistance and the cancer stem-like cell phenotype of lung cancer, and these results suggest that targeting the NF-κB/miR-590/EHD1 pathway has potential therapeutic promise in EGFR-mutant NSCLC patients with acquired EGFR-TKI resistance.

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Metadata

Authors
Wang, X., Yin, H., Zhang, H., Hu, J., Lu, H., Li, C., Cao, M., Yan, S., & Cai, L.
Venue
Cell Death & Disease
Publisher
Springer Science and Business Media LLC
Published
2018-03-16
Volume
9
Issue
4
ISSN
2041-4889
DOI
10.1038/s41419-018-0447-7
PMC
PMC5856828
Cited by
31
References
1
Language
en
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