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Open AccessReview

Targeting Autophagy for Overcoming Resistance to Anti-EGFR Treatments

1
Department of Biochemistry, College of Natural Sciences, Kangwon National University, Chunchon 24341, Korea
2
Institute of New Frontier Research, College of Medicine, Hallym University, Chunchon 24251, Korea
*
Author to whom correspondence should be addressed.
Cancers 2019, 11(9), 1374; https://doi.org/10.3390/cancers11091374
Received: 29 July 2019 / Revised: 30 August 2019 / Accepted: 10 September 2019 / Published: 16 September 2019
(This article belongs to the Special Issue Epidermal Growth Factor Receptor Signaling in Cancer)
Epidermal growth factor receptor (EGFR) plays critical roles in cell proliferation, tumorigenesis, and anti-cancer drug resistance. Overexpression and somatic mutations of EGFR result in enhanced cancer cell survival. Therefore, EGFR can be a target for the development of anti-cancer therapy. Patients with cancers, including non-small cell lung cancers (NSCLC), have been shown to response to EGFR-tyrosine kinase inhibitors (EGFR-TKIs) and anti-EGFR antibodies. However, resistance to these anti-EGFR treatments has developed. Autophagy has emerged as a potential mechanism involved in the acquired resistance to anti-EGFR treatments. Anti-EGFR treatments can induce autophagy and result in resistance to anti-EGFR treatments. Autophagy is a programmed catabolic process stimulated by various stimuli. It promotes cellular survival under these stress conditions. Under normal conditions, EGFR-activated phosphoinositide 3-kinase (PI3K)/AKT serine/threonine kinase (AKT)/mammalian target of rapamycin (mTOR) signaling inhibits autophagy while EGFR/rat sarcoma viral oncogene homolog (RAS)/mitogen-activated protein kinase kinase (MEK)/mitogen-activated protein kinase (MAPK) signaling promotes autophagy. Thus, targeting autophagy may overcome resistance to anti-EGFR treatments. Inhibitors targeting autophagy and EGFR signaling have been under development. In this review, we discuss crosstalk between EGFR signaling and autophagy. We also assess whether autophagy inhibition, along with anti-EGFR treatments, might represent a promising approach to overcome resistance to anti-EGFR treatments in various cancers. In addition, we discuss new developments concerning anti-autophagy therapeutics for overcoming resistance to anti-EGFR treatments in various cancers. View Full-Text
Keywords: anti-EGFR treatments; autophagy; EGFR signaling; co-targeting anti-EGFR treatments; autophagy; EGFR signaling; co-targeting
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MDPI and ACS Style

Kwon, Y.; Kim, M.; Jung, H.S.; Kim, Y.; Jeoung, D. Targeting Autophagy for Overcoming Resistance to Anti-EGFR Treatments. Cancers 2019, 11, 1374. https://doi.org/10.3390/cancers11091374

AMA Style

Kwon Y, Kim M, Jung HS, Kim Y, Jeoung D. Targeting Autophagy for Overcoming Resistance to Anti-EGFR Treatments. Cancers. 2019; 11(9):1374. https://doi.org/10.3390/cancers11091374

Chicago/Turabian Style

Kwon, Yoojung; Kim, Misun; Jung, Hyun S.; Kim, Youngmi; Jeoung, Dooil. 2019. "Targeting Autophagy for Overcoming Resistance to Anti-EGFR Treatments" Cancers 11, no. 9: 1374. https://doi.org/10.3390/cancers11091374

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Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

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