دورية أكاديمية
أعرض في EDS

ASPM stabilizes the NOTCH intracellular domain 1 and promotes oncogenesis by blocking FBXW7 binding in hepatocellular carcinoma cells.

التفاصيل البيبلوغرافية
العنوان: ASPM stabilizes the NOTCH intracellular domain 1 and promotes oncogenesis by blocking FBXW7 binding in hepatocellular carcinoma cells.
المؤلفون: Chan TS; Laboratory of Advanced Molecular Therapeutics, Graduate Institute of Clinical Medicine, College of Medicine, Taipei Medical University, Taiwan.; Division of Gastroenterology, Department of Internal Medicine, Wan Fang Hospital, Taipei Medical University, Taiwan.; School of Medicine, College of Medicine, Taipei Medical University, Taiwan.; Pancreatic Cancer Group, Taipei Cancer Center, Taipei Medical University, Taiwan., Cheng LH; Laboratory of Advanced Molecular Therapeutics, Graduate Institute of Clinical Medicine, College of Medicine, Taipei Medical University, Taiwan.; Core Laboratory of Organoids Technology, Office of R&D, Taipei Medical University, Taiwan., Hsu CC; School of Medicine, College of Medicine, I-Shou University, Kaohsiung City, Taiwan., Yang PM; Master Program in Graduate Institute of Cancer Biology and Drug Discovery, Taipei Medical University, Taiwan., Liao TY; Laboratory of Advanced Molecular Therapeutics, Graduate Institute of Clinical Medicine, College of Medicine, Taipei Medical University, Taiwan., Hsieh HY; Laboratory of Advanced Molecular Therapeutics, Graduate Institute of Clinical Medicine, College of Medicine, Taipei Medical University, Taiwan., Lin PC; Laboratory of Advanced Molecular Therapeutics, Graduate Institute of Clinical Medicine, College of Medicine, Taipei Medical University, Taiwan., HuangFu WC; Master Program in Graduate Institute of Cancer Biology and Drug Discovery, Taipei Medical University, Taiwan., Chuu CP; Institute of Cellular and System Medicine, National Health Research Institutes, Miaoli, Taiwan., Tsai KK; Laboratory of Advanced Molecular Therapeutics, Graduate Institute of Clinical Medicine, College of Medicine, Taipei Medical University, Taiwan.; Division of Gastroenterology, Department of Internal Medicine, Wan Fang Hospital, Taipei Medical University, Taiwan.; Pancreatic Cancer Group, Taipei Cancer Center, Taipei Medical University, Taiwan.; Core Laboratory of Organoids Technology, Office of R&D, Taipei Medical University, Taiwan.; TMU Research Center of Cancer Translational Medicine, Taipei Medical University, Taiwan.
المصدر: Molecular oncology [Mol Oncol] 2024 Mar; Vol. 18 (3), pp. 562-579. Date of Electronic Publication: 2024 Jan 26.
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
مواضيع طبية MeSH: Carcinoma, Hepatocellular*/pathology , F-Box Proteins*/genetics , F-Box Proteins*/metabolism , Liver Neoplasms*/pathology, Humans ; Cell Line, Tumor ; F-Box-WD Repeat-Containing Protein 7/genetics ; Nerve Tissue Proteins/metabolism ; Receptor, Notch1/genetics ; Receptor, Notch1/metabolism
مستخلص: Notch signaling is aberrantly activated in approximately 30% of hepatocellular carcinoma (HCC), significantly contributing to tumorigenesis and disease progression. Expression of the major Notch receptor, NOTCH1, is upregulated in HCC cells and correlates with advanced disease stages, although the molecular mechanisms underlying its overexpression remain unclear. Here, we report that expression of the intracellular domain of NOTCH1 (NICD1) is upregulated in HCC cells due to antagonism between the E3-ubiquitin ligase F-box/WD repeat-containing protein 7 (FBXW7) and the large scaffold protein abnormal spindle-like microcephaly-associated protein (ASPM) isoform 1 (ASPM-i1). Mechanistically, FBXW7-mediated polyubiquitination and the subsequent proteasomal degradation of NICD1 are hampered by the interaction of NICD1 with ASPM-i1, thereby stabilizing NICD1 and rendering HCC cells responsive to stimulation by Notch ligands. Consistently, downregulating ASPM-i1 expression reduced the protein abundance of NICD1 but not its FBXW7-binding-deficient mutant. Reinforcing the oncogenic function of this regulatory module, the forced expression of NICD1 significantly restored the tumorigenic potential of ASPM-i1-deficient HCC cells. Echoing these findings, NICD1 was found to be strongly co-expressed with ASPM-i1 in cancer cells in human HCC tissues (P < 0.001). In conclusion, our study identifies a novel Notch signaling regulatory mechanism mediated by protein-protein interaction between NICD1, FBXW7, and ASPM-i1 in HCC cells, representing a targetable vulnerability in human HCC.
(© 2024 The Authors. Molecular Oncology published by John Wiley & Sons Ltd on behalf of Federation of European Biochemical Societies.)
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معلومات مُعتمدة: 112-WF-SWF-01 Wan Fang Hospital, Taipei Medical University; 109-TMU-WFH-05 Taipei Medical University; DP2-107-21121-C-04 Taipei Medical University; DP2-TMU-112-0-12 Taipei Medical University; TMU106-AE1-B31 Taipei Medical University; MOST 108-2314-B-038-105 National Science and Technology Council, Taiwan (R.O.C.); MOST 109-2314-B-038-130 National Science and Technology Council, Taiwan (R.O.C.); MOST 111-2314-B-038-075 National Science and Technology Council, Taiwan (R.O.C.); MOST 111-2320-B-038-021 National Science and Technology Council, Taiwan (R.O.C.); MOST 111-2327-B-038-001 National Science and Technology Council, Taiwan (R.O.C.); NSTC112-2823-8-038-004 National Science and Technology Council, Taiwan (R.O.C.)
فهرسة مساهمة: Keywords: ASPM; FBXW7; NOTCH1; Notch signaling; hepatocellular carcinoma; tumorigenesis
سلسلة جزيئية: RefSeq NP_060606.3; NP_001193775.1; NM_018136.4
المشرفين على المادة: 0 (ASPM protein, human)
0 (F-Box Proteins)
0 (F-Box-WD Repeat-Containing Protein 7)
0 (FBXW7 protein, human)
0 (Nerve Tissue Proteins)
0 (Receptor, Notch1)
0 (NOTCH1 protein, human)
تواريخ الأحداث: Date Created: 20240127 Date Completed: 20240311 Latest Revision: 20240313
رمز التحديث: 20240313
مُعرف محوري في PubMed: PMC10920086
DOI: 10.1002/1878-0261.13589
PMID: 38279565
قاعدة البيانات: MEDLINE
الوصف
تدمد:1878-0261
DOI:10.1002/1878-0261.13589