1. Living Beyond Restriction: LBR promotes cellular immortalization by suppressing genomic instability and senescence.
- Author
-
Choi H and Kang C
- Subjects
- Humans, Receptors, Cytoplasmic and Nuclear genetics, Receptors, Cytoplasmic and Nuclear metabolism, Animals, Retinoblastoma Protein genetics, Retinoblastoma Protein metabolism, Neoplasms genetics, Neoplasms pathology, Neoplasms metabolism, Cell Proliferation genetics, Cell Transformation, Neoplastic genetics, Cell Transformation, Neoplastic metabolism, Cell Transformation, Neoplastic pathology, Cellular Senescence genetics, Genomic Instability, Tumor Suppressor Protein p53 genetics, Tumor Suppressor Protein p53 metabolism, Lamin B Receptor
- Abstract
Cellular immortalization is a complex process that requires multiple genetic alterations to overcome restricting barriers, including senescence. Not surprisingly, many of these alterations are associated with cancer; two tumor suppressor pathways, the cellular tumor antigen p53 and p16-Retinoblastoma (RB) pathways, are the best-characterized examples, but their mutations alone are known to be insufficient to drive full immortalization. En et al. identified a role for the lamin B receptor (LBR) in promoting cellular proliferation and immortalization in p53- and RB-deficient cells by maintaining their genome integrity and suppressing senescence. Thus, modulation of LBR could be exploited to treat cancer and potentially also to promote cell rejuvenation., (© 2024 The Authors. The FEBS Journal published by John Wiley & Sons Ltd on behalf of Federation of European Biochemical Societies.)
- Published
- 2024
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