دورية أكاديمية
أعرض في EDS

Upregulated expression of lamin B receptor increases cell proliferation and suppresses genomic instability: implications for cellular immortalization.

التفاصيل البيبلوغرافية
العنوان: Upregulated expression of lamin B receptor increases cell proliferation and suppresses genomic instability: implications for cellular immortalization.
المؤلفون: En A; Graduate School of Nanobioscience, Yokohama City University, Japan., Takemoto K; Graduate School of Nanobioscience, Yokohama City University, Japan., Yamakami Y; Graduate School of Nanobioscience, Yokohama City University, Japan., Nakabayashi K; Department of Maternal-Fetal Biology, National Center for Child Health and Development, Tokyo, Japan., Fujii M; Graduate School of Nanobioscience, Yokohama City University, Japan.
المصدر: The FEBS journal [FEBS J] 2024 May; Vol. 291 (10), pp. 2155-2171. Date of Electronic Publication: 2024 Mar 11.
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: Published by Blackwell Pub. on behalf of the Federation of European Biochemical Societies Country of Publication: England NLM ID: 101229646 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1742-4658 (Electronic) Linking ISSN: 1742464X NLM ISO Abbreviation: FEBS J Subsets: MEDLINE
أسماء مطبوعة: Original Publication: Oxford, UK : Published by Blackwell Pub. on behalf of the Federation of European Biochemical Societies, c2005-
مواضيع طبية MeSH: Cell Proliferation*/genetics , Cellular Senescence*/genetics , Genomic Instability*/genetics , Lamin B Receptor* , Receptors, Cytoplasmic and Nuclear*/genetics , Receptors, Cytoplasmic and Nuclear*/metabolism, Humans ; Antigens, Polyomavirus Transforming/genetics ; Antigens, Polyomavirus Transforming/metabolism ; Fibroblasts/metabolism ; Heterochromatin/genetics ; Heterochromatin/metabolism ; Lamin Type A/genetics ; Lamin Type A/metabolism ; Lamin Type B/genetics ; Lamin Type B/metabolism ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Protein p53/metabolism ; Up-Regulation
مستخلص: Mammalian somatic cells undergo terminal proliferation arrest after a limited number of cell divisions, a phenomenon termed cellular senescence. However, cells acquire the ability to proliferate infinitely (cellular immortalization) through multiple genetic alterations. Inactivation of tumor suppressor genes such as p53, RB and p16 is important for cellular immortalization, although additional molecular alterations are required for cellular immortalization to occur. Here, we aimed to gain insights into these molecular alterations. Given that cellular immortalization is the escape of cells from cellular senescence, genes that regulate cellular senescence are likely to be involved in cellular immortalization. Because senescent cells show altered heterochromatin organization, we investigated the implications of lamin A/C, lamin B1 and lamin B receptor (LBR), which regulate heterochromatin organization, in cellular immortalization. We employed human immortalized cell lines, KMST-6 and SUSM-1, and found that expression of LBR was upregulated upon cellular immortalization and downregulated upon cellular senescence. In addition, knockdown of LBR induced cellular senescence with altered chromatin configuration. Additionally, enforced expression of LBR increased cell proliferation likely through suppression of genome instability in human primary fibroblasts that expressed the simian virus 40 large T antigen (TAg), which inactivates p53 and RB. Furthermore, expression of TAg or knockdown of p53 led to upregulated LBR expression. These observations suggested that expression of LBR might be upregulated to suppress genome instability in TAg-expressing cells, and, consequently, its upregulated expression assisted the proliferation of TAg-expressing cells (i.e. p53/RB-defective cells). Our findings suggest a crucial role for LBR in the process of cellular immortalization.
(© 2024 Federation of European Biochemical Societies.)
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معلومات مُعتمدة: 22K11730 Ministry of Education, Culture, Sports, Science and Technology
فهرسة مساهمة: Keywords: cellular immortalization; cellular senescence; heterochromatin; lamin B receptor
المشرفين على المادة: 0 (Antigens, Polyomavirus Transforming)
0 (Heterochromatin)
0 (Lamin B Receptor)
0 (Lamin Type A)
0 (Lamin Type B)
0 (Receptors, Cytoplasmic and Nuclear)
0 (Tumor Suppressor Protein p53)
تواريخ الأحداث: Date Created: 20240311 Date Completed: 20240516 Latest Revision: 20240809
رمز التحديث: 20240812
DOI: 10.1111/febs.17113
PMID: 38462947
قاعدة البيانات: MEDLINE
الوصف
تدمد:1742-4658
DOI:10.1111/febs.17113