دورية أكاديمية
أعرض في EDS

Context matters - Daxx and Atrx are not robust tumor suppressors in the murine endocrine pancreas.

التفاصيل البيبلوغرافية
العنوان: Context matters - Daxx and Atrx are not robust tumor suppressors in the murine endocrine pancreas.
المؤلفون: Sun C; Department of Genetics, The University of Texas MD Anderson Cancer Center, Houston, TX, 77030USA.; Genetics and Epigenetics Program, The University of Texas MD Anderson Cancer Center UTHealth Graduate School of Biomedical Sciences, Houston, TX 77030, USA., Estrella JS; Department of Anatomic Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA., Whitley EM; Department of Veterinary Medicine and Surgery, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA., Chau GP; Department of Genetics, The University of Texas MD Anderson Cancer Center, Houston, TX, 77030USA., Lozano G; Department of Genetics, The University of Texas MD Anderson Cancer Center, Houston, TX, 77030USA.; Genetics and Epigenetics Program, The University of Texas MD Anderson Cancer Center UTHealth Graduate School of Biomedical Sciences, Houston, TX 77030, USA., Wasylishen AR; Department of Genetics, The University of Texas MD Anderson Cancer Center, Houston, TX, 77030USA.
المصدر: Disease models & mechanisms [Dis Model Mech] 2022 Aug 01; Vol. 15 (8). Date of Electronic Publication: 2022 Aug 26.
نوع المنشور: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: Company of Biologists Ltd Country of Publication: England NLM ID: 101483332 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1754-8411 (Electronic) Linking ISSN: 17548403 NLM ISO Abbreviation: Dis Model Mech Subsets: MEDLINE
أسماء مطبوعة: Original Publication: Cambridge : Company of Biologists Ltd., c2008-
مواضيع طبية MeSH: Islets of Langerhans*/pathology , Neuroendocrine Tumors*/genetics , Pancreatic Neoplasms*/genetics , Pancreatic Neoplasms*/pathology, Adaptor Proteins, Signal Transducing/genetics ; Adaptor Proteins, Signal Transducing/metabolism ; Animals ; Carcinogenesis ; Co-Repressor Proteins ; DNA Helicases ; Humans ; Mental Retardation, X-Linked ; Mice ; Molecular Chaperones ; Nuclear Proteins/genetics ; Nuclear Proteins/metabolism ; X-linked Nuclear Protein/genetics ; alpha-Thalassemia
مستخلص: Genome sequencing has revealed the importance of epigenetic regulators in tumorigenesis. The genes encoding the chromatin remodeling complex DAXX:ATRX are frequently mutated in pancreatic neuroendocrine tumors; however, the underlying mechanisms of how mutations contribute to tumorigenesis are only partially understood, in part because of the lack of relevant preclinical models. Here, we used genetically engineered mouse models combined with environmental stress to evaluate the tumor suppressor functions of Daxx and Atrx in the mouse pancreas. Daxx or Atrx loss, alone or in combination with Men1 loss, did not drive or accelerate pancreatic neuroendocrine tumorigenesis. Moreover, Daxx loss did not cooperate with environmental stresses (ionizing radiation or pancreatitis) or with the loss of other tumor suppressors (Pten or p53) to promote pancreatic neuroendocrine tumorigenesis. However, owing to promiscuity of the Cre promoter used, hepatocellular carcinomas and osteosarcomas were observed in some instances. Overall, our findings suggest that Daxx and Atrx are not robust tumor suppressors in the endocrine pancreas of mice and indicate that the context of a human genome is essential for tumorigenesis. This article has an associated First Person interview with the first author of the paper.
Competing Interests: Competing interests The authors declare no competing or financial interests.
(© 2022. Published by The Company of Biologists Ltd.)
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معلومات مُعتمدة: P30 CA016672 United States CA NCI NIH HHS; R21 CA208463 United States CA NCI NIH HHS; Canada CIHR
فهرسة مساهمة: Keywords: Atrx; Daxx; Men1; Mouse model; Pancreatic neuroendocrine tumor
المشرفين على المادة: 0 (Adaptor Proteins, Signal Transducing)
0 (Co-Repressor Proteins)
0 (DAXX protein, human)
0 (Daxx protein, mouse)
0 (Molecular Chaperones)
0 (Nuclear Proteins)
EC 3.6.4.- (DNA Helicases)
EC 3.6.4.12 (ATRX protein, human)
EC 3.6.4.12 (Atrx protein, mouse)
EC 3.6.4.12 (X-linked Nuclear Protein)
SCR Disease Name: ATR-X syndrome
تواريخ الأحداث: Date Created: 20220817 Date Completed: 20220829 Latest Revision: 20220910
رمز التحديث: 20231215
مُعرف محوري في PubMed: PMC9438929
DOI: 10.1242/dmm.049552
PMID: 35976056
قاعدة البيانات: MEDLINE
الوصف
تدمد:1754-8411
DOI:10.1242/dmm.049552