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Functional loss of ERBB receptor feedback inhibitor 1 (MIG6) promotes glioblastoma tumorigenesis by aberrant activation of epidermal growth factor receptor (EGFR).

التفاصيل البيبلوغرافية
العنوان: Functional loss of ERBB receptor feedback inhibitor 1 (MIG6) promotes glioblastoma tumorigenesis by aberrant activation of epidermal growth factor receptor (EGFR).
المؤلفون: Yi SA; Epigenome Dynamics Control Research Center, School of Pharmacy, Sungkyunkwan University, Suwon, Korea., Cho D; Department of Biomedical Science & Engineering, Dankook University, Cheonan, Korea.; Department of Nanobiomedical Science, Dankook University, Cheonan, Korea., Kim S; Department of Biomedical Science & Engineering, Dankook University, Cheonan, Korea.; Department of Nanobiomedical Science, Dankook University, Cheonan, Korea., Kim H; Department of Nanobiomedical Science, Dankook University, Cheonan, Korea., Choi MK; Department of Systems Biology, College of Life Science and Biotechnology, Yonsei University, Seoul, Korea., Choi HS; Department of Systems Biology, College of Life Science and Biotechnology, Yonsei University, Seoul, Korea., Shin S; Department of Biomedical Science & Engineering, Dankook University, Cheonan, Korea.; Department of Nanobiomedical Science, Dankook University, Cheonan, Korea., Yun S; Department of Biomedical Science & Engineering, Dankook University, Cheonan, Korea.; Department of Nanobiomedical Science, Dankook University, Cheonan, Korea., Lim A; Department of Biomedical Science & Engineering, Dankook University, Cheonan, Korea.; Department of Nanobiomedical Science, Dankook University, Cheonan, Korea., Jeong JK; Department of Nanobiomedical Science, Dankook University, Cheonan, Korea., Yoon DE; Department of Biomedical Sciences, Korea University College of Medicine, Seoul, Korea.; Department of Physiology, Korea University College of Medicine, Seoul, Korea., Cha HJ; Department of Biomedical Science & Engineering, Dankook University, Cheonan, Korea., Kim K; Department of Biomedical Sciences, Korea University College of Medicine, Seoul, Korea.; Department of Physiology, Korea University College of Medicine, Seoul, Korea., Han JW; Epigenome Dynamics Control Research Center, School of Pharmacy, Sungkyunkwan University, Suwon, Korea., Cho HS; Department of Systems Biology, College of Life Science and Biotechnology, Yonsei University, Seoul, Korea., Cho J; Department of Biomedical Science & Engineering, Dankook University, Cheonan, Korea.; Department of Nanobiomedical Science, Dankook University, Cheonan, Korea.
المصدر: Molecular oncology [Mol Oncol] 2024 Aug 11. Date of Electronic Publication: 2024 Aug 11.
Publication Model: Ahead of Print
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: John Wiley & Sons, Inc Country of Publication: United States NLM ID: 101308230 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1878-0261 (Electronic) Linking ISSN: 15747891 NLM ISO Abbreviation: Mol Oncol Subsets: MEDLINE
أسماء مطبوعة: Publication: 2017- : Hoboken, New Jersey : John Wiley & Sons, Inc.
Original Publication: Amsterdam : Elsevier
مستخلص: Dysregulation of epidermal growth factor receptor (EGFR) is one of the most common mechanisms associated with the pathogenesis of various cancers. Mitogen-inducible gene 6 [MIG6; also known as ERBB receptor feedback inhibitor 1 (ERRFI1)], identified as a feedback inhibitor of EGFR, negatively regulates EGFR by directly inhibiting its kinase activity and facilitating its internalization, subsequently leading to degradation. Despite its proposed role as an EGFR-dependent tumor suppressor, the functional consequences and clinical relevance in cancer etiology remain incompletely understood. Here, we identify that the stoichiometric balance between MIG6 and EGFR is crucial in promoting EGFR-dependent oncogenic growth in various experimental model systems. In addition, a subset of ERRFI1 (the official gene symbol of MIG6) mutations exhibit impaired ability to suppress the enzymatic activation of EGFR at multiple levels. In summary, our data suggest that decreased or loss of MIG6 activity can lead to abnormal activation of EGFR, potentially contributing to cellular transformation. We propose that the mutation status of ERRFI1 and the expression levels of MIG6 can serve as additional biomarkers for guiding EGFR-targeted cancer therapies, including glioblastoma.
(© 2024 The Author(s). Molecular Oncology published by John Wiley & Sons Ltd on behalf of Federation of European Biochemical Societies.)
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معلومات مُعتمدة: 2019M3E5D6063903 National Research Foundation of Korea; 2021R1A2C3010506 National Research Foundation of Korea; 2017R1A2B3002186 National Research Foundation of Korea; 2019R1A5A2027340 National Research Foundation of Korea; 2016R1A2B2011100 National Research Foundation of Korea; 2019R1A4A1028268 National Research Foundation of Korea; 2017R1A6A3A04001986 National Research Foundation of Korea
فهرسة مساهمة: Keywords: EGFR; MIG6; biomarker; glioblastoma (GBM); targeted cancer therapy
تواريخ الأحداث: Date Created: 20240812 Latest Revision: 20240812
رمز التحديث: 20240813
DOI: 10.1002/1878-0261.13717
PMID: 39129344
قاعدة البيانات: MEDLINE
الوصف
تدمد:1878-0261
DOI:10.1002/1878-0261.13717