Pathways driving the endocytosis of mutant and wild-type EGFR in cancer
Open accessAbstract
EGFR (epidermal growth factor receptor) is activated through changes in expression or mutations in a number of tumors and is a driving force in cancer progression. EGFR is targeted by numerous inhibitors, including chimeric antibodies targeting the extracellular domain and small molecule kinase domain inhibitors. The kinase domain inhibitors are particularly active against mutant forms of the receptor, and subsequent mutations drive resistance to the inhibitors. Here, we review recent developments on the trafficking of wild-type and mutant EGFR, focusing on the roles of MIG6, SPRY2, ITSN, SHP2, S2R(PGRMC1) and RAK. Some classes of EGFR regulators affect wild-type and mutant EGFR equally, while others are specific for either the wild-type or mutant form of the receptor. Below we summarize multiple signaling-associated pathways that are important in trafficking wild-type and mutant EGFR with the goal being stimulation of new approaches for targeting the distinct forms of the receptor.
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Mutant forms of EGFR have different trafficking compared with the wild type receptor, because some regulatory proteins that balance the EGFR pathway have altered expression in cancer.
“Mutant forms of EGFR have different trafficking compared with the wild type receptor, since some of the regulatory proteins that balance the EGFR pathway present altered expression in cancer [4].”
From A decade of EGFR inhibition in EGFR-mutated non small cell lung cancer (NSCLC): Old successes and future perspectives (2015) · cites this paper as [4]
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References 96 · Cited by 35
Research works printed but not linked: 1
- [32]Rohe HJ Ahmed IS Twist KE Craven RJ PGRMC1: a targetable protein with multiple functions in steroid signaling, P450 activation and drug binding Pharmacol Ther 2009 121 14 19 18992768 PMC2659782
- Authors
- Hampton, K. K., & Craven, R. J.
- Affiliations
- University of Kentucky (US)
- Corresponding author
- Craven, Rolf J.
- ORCID
- Hampton, Kaia K.
- Venue
- Oncoscience
- Publisher
- Impact Journals, LLC
- Published
- 2014-07-29
- Volume
- 1
- Issue
- 8
- Pages
- 504-512
- ISSN
- 2331-4737 (ISSN-L)
- PMC
- PMC4278327
- OpenAlex
- W2260089498
- Cited by
- 35
- References
- 96
- Citations by year
- 2024: 5 · 2023: 3 · 2022: 3 · 2021: 2 · 2020: 2 · 2019: 1 · 2018: 5 · 2017: 2 · 2016: 6 · 2015: 6
- FWCI
- 2.25
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Oncoscience (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Oncology › HER2/EGFR in Cancer Research
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Lung Cancer Treatments and Mutations
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Cellular transport and secretion
- Keywords
- EGFR, endocytosis, receptor trafficking, mutant EGFR, EGFR wild-type, EGFR kinase inhibitors, inhibitor resistance, MIG6, SPRY2, SHP2, PGRMC1, RAK, tumor progression, receptor internalization
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