دورية أكاديمية
أعرض في EDS

MYC selects against reduced BCL2A1/A1 protein expression during B cell lymphomagenesis.

التفاصيل البيبلوغرافية
العنوان: MYC selects against reduced BCL2A1/A1 protein expression during B cell lymphomagenesis.
المؤلفون: Sochalska M; Division of Developmental Immunology, Biocenter, Medical University of Innsbruck, Innsbruck, Austria., Schuler F; Division of Developmental Immunology, Biocenter, Medical University of Innsbruck, Innsbruck, Austria., Weiss JG; Division of Developmental Immunology, Biocenter, Medical University of Innsbruck, Innsbruck, Austria., Prchal-Murphy M; Institute of Pharmacology and Toxicology, Department of Biomedical Sciences, University of Veterinary Medicine, Vienna, Austria., Sexl V; Institute of Pharmacology and Toxicology, Department of Biomedical Sciences, University of Veterinary Medicine, Vienna, Austria., Villunger A; Division of Developmental Immunology, Biocenter, Medical University of Innsbruck, Innsbruck, Austria.; Tyrolean Cancer Research Institute, Innsbruck, Austria.
المصدر: Oncogene [Oncogene] 2017 Apr; Vol. 36 (15), pp. 2066-2073. Date of Electronic Publication: 2016 Oct 03.
نوع المنشور: Journal Article; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: Nature Publishing Group Country of Publication: England NLM ID: 8711562 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1476-5594 (Electronic) Linking ISSN: 09509232 NLM ISO Abbreviation: Oncogene Subsets: MEDLINE
أسماء مطبوعة: Publication: <2002->: Basingstoke : Nature Publishing Group
Original Publication: Basingstoke, Hampshire, UK : Scientific & Medical Division, MacMillan Press, c1987-
مواضيع طبية MeSH: Lymphoma, B-Cell/*genetics , Minor Histocompatibility Antigens/*genetics , Proto-Oncogene Proteins c-bcl-2/*genetics , Proto-Oncogene Proteins c-myc/*genetics, Animals ; Apoptosis/genetics ; Cell Line, Tumor ; Cell Transformation, Neoplastic ; Gene Expression Regulation, Neoplastic ; Gene Knockdown Techniques ; Lymphoma, B-Cell/metabolism ; Lymphoma, B-Cell/pathology ; Mice ; Mice, Transgenic ; Minor Histocompatibility Antigens/biosynthesis ; Precursor Cell Lymphoblastic Leukemia-Lymphoma/genetics ; Precursor Cell Lymphoblastic Leukemia-Lymphoma/metabolism ; Precursor Cell Lymphoblastic Leukemia-Lymphoma/pathology ; Proto-Oncogene Proteins c-bcl-2/biosynthesis ; Proto-Oncogene Proteins c-myc/biosynthesis
مستخلص: Rearrangements of MYC or ABL proto-oncogenes lead to deregulated expression of key-regulators of cell cycle and cell survival, thereby constituting important drivers of blood cancer. Members of the BCL-2 family of apoptosis regulators contribute to oncogenic transformation downstream of these oncogenes, but the role of anti-apoptotic BCL2A1/A1 in transformation and drug resistance caused by deregulation of these oncogenes remains enigmatic. Here we analyzed the role of A1 in MYC as well as ABL kinase-driven blood cancer in mice, employing in vivo RNAi. We report that overexpression of either oncogene leads to a significant increase in A1 protein levels in otherwise A1-negative B cell progenitors, indicating a key role downstream of these oncogenes to secure survival during transformation. Knockdown of A1 by RNAi, however, did not impact on tumor latency in v-Abl-driven pre-B-ALL. In contrast, A1 knockdown in premalignant Eμ-MYC mice caused a significant reduction of transgenic pre-B cells without impacting on tumor latency as the emerging lymphomas escaped silencing of A1 expression. These findings identify A1 as a MYC target that can be induced prematurely during B cell development to aid expansion of otherwise cell-death-prone MYC transgenic pre-B cells. Hence, A1 should be considered as a putative drug target in MYC-driven blood cancer.
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المشرفين على المادة: 0 (BCL2-related protein A1)
0 (Minor Histocompatibility Antigens)
0 (Myc protein, mouse)
0 (Proto-Oncogene Proteins c-bcl-2)
0 (Proto-Oncogene Proteins c-myc)
تواريخ الأحداث: Date Created: 20161004 Date Completed: 20170419 Latest Revision: 20210109
رمز التحديث: 20240628
مُعرف محوري في PubMed: PMC5395700
DOI: 10.1038/onc.2016.362
PMID: 27694901
قاعدة البيانات: MEDLINE
الوصف
تدمد:1476-5594
DOI:10.1038/onc.2016.362