The role of nuclear lamin B1 in cell proliferation and senescence
Open accessAbstract
Nuclear lamin B1 (LB1) is a major structural component of the nucleus that appears to be involved in the regulation of many nuclear functions. The results of this study demonstrate that LB1 expression in WI-38 cells decreases during cellular senescence. Premature senescence induced by oncogenic Ras also decreases LB1 expression through a retinoblastoma protein (pRb)-dependent mechanism. Silencing the expression of LB1 slows cell proliferation and induces premature senescence in WI-38 cells. The effects of LB1 silencing on proliferation require the activation of p53, but not pRb. However, the induction of premature senescence requires both p53 and pRb. The proliferation defects induced by silencing LB1 are accompanied by a p53-dependent reduction in mitochondrial reactive oxygen species (ROS), which can be rescued by growth under hypoxic conditions. In contrast to the effects of LB1 silencing, overexpression of LB1 increases the proliferation rate and delays the onset of senescence of WI-38 cells. This overexpression eventually leads to cell cycle arrest at the G1/S boundary. These results demonstrate the importance of LB1 in regulating the proliferation and senescence of human diploid cells through a ROS signaling pathway.
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Cellular senescence is accompanied by substantial reorganization of the nuclear envelope and a breakdown in nucleocytoplasmic trafficking, including altered expression and degradation of Lamin B1, and formation of cytoplasmic chromatin fragments.
“Cellular senescence is accompanied by substantial reorganization of the nuclear envelope and a breakdown in nucleocytoplasmic trafficking, including altered expression and degradation of Lamin B1, and the formation of cytoplasmic chromatin fragments (CCFs) [38–45].”
From Chemically induced reprogramming to reverse cellular aging (2023) · cites this paper as [45]
Split into 2 atoms — 0 confirmed, 2 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
Experimental — accuracy not yet measuredDepletion of LMNB1 is sufficient to induce senescence through modulation of reactive oxygen species (ROS) production.
“Shimi et al. (2011) showed that depletion of LMNB1 is sufficient to induce senescence through modulation of reactive oxygen species (ROS) production.”
From Cellular senescence and its effector programs (2014) · cites this paper as Shimi et al. 2011
The section ‘LB1 silencing inhibits proliferation and induces premature senescence’ reports that silencing LB1 induced senescence in the human fibroblasts studied. The ROS-signaling section reports an early decrease in ROS and says the results ‘suggest’ that a ROS pathway is responsible for induction of the senescence program. The claim presents that proposed mechanism as established and omits the study’s cell-type scope. (LLM, conf=0.84)
Experimental — accuracy not yet measuredLamin B1 (LMNB1) is specifically down-regulated during senescence in human diploid fibroblasts (HDFs).
“Recently, Lamin B1 (LMNB1) was reported to be specifically down-regulated during senescence in HDFs (Shimi et al. 2011).”
From Cellular senescence and its effector programs (2014) · cites this paper as Shimi et al. 2011
Depletion of LMNB1 leads to a reduction of ROS in a p53-dependent manner.
“Perhaps paradoxically, they showed that depletion of LMNB1 leads to a reduction of ROS in a p53-depenent manner.”
From Cellular senescence and its effector programs (2014) · cites this paper as Shimi et al. 2011
RNAi-mediated depletion of LMNB1 is associated with reduced cell proliferation to various degrees in most studies.
“However, RNAi-mediated depletion of LMNB1 appears to be associated with reduced cell proliferation to various degrees in most (Shimi et al. 2011; Dreesen et al. 2013; Sadaie et al. 2013; Shah et al. 2013).”
From Cellular senescence and its effector programs (2014) · cites this paper as Shimi et al. 2011
Overexpression of LMNB1 either delays or enhances senescence or exhibits minimal effect on proliferation, depending on study.
“Compared with LMNB1 depletion, phenotypes induced by ectopic LMNB1 were more heterogeneous between studies: Overexpression of LMNB1 either delays (Shimi et al. 2011) or enhances senescence (Barascu et al. 2012; Dreesen et al. 2013) or exhibits a minimal effect on proliferation (Sadaie et al. 2013).”
From Cellular senescence and its effector programs (2014) · cites this paper as Shimi et al. 2011
Genome-wide analysis of H3K4me3, H3K27me3 and H3K27ac in senescent cells reveals dynamic acquisition and depletion of large-scale chromatin domains proposed to regulate key senescence downstream effectors.
“Genome-wide analysis of H3 Lys4 trimethylation, H3 Lys27 trimethylation and H3 Lys27 acetylation in senescent cells has also revealed the dynamic acquisition and depletion of large-scale chromatin domains that have been proposed to regulate the expression of key senescence downstream effectors68–72”
From Cellular senescence in ageing: from mechanisms to therapeutic opportunities (2021) · cites this paper as [70]
The Discussion proposes that lamin B1 might affect chromatin organization and gene expression, and the methods describe a targeted senescence-gene expression assay. Our copy does not report a genome-wide analysis of H3K4me3, H3K27me3, or H3K27ac, or the acquisition and depletion of large-scale domains; searches for those marks and domain changes found no supporting passage. No page numbers were available in the indexed passages. (LLM, conf=0.74)
Experimental — accuracy not yet measuredLoss of Lamin B1 is a well-known feature of cell senescence.
“Loss of Lamin B1 is a well-known feature of cell senescence (Freund et al., 2012; Shimi et al., 2011).”
From Cytoplasmic DNA: sources, sensing, and role in aging and disease (2021) · cites this paper as Shimi et al., 2011
Overexpression of Lamin B1 delays senescence onset, suggesting Lamin B1 loss may be upstream of CCF formation.
“while the overexpression of Lamin B1 delays onset of senescence (Shimi et al., 2011), suggesting that Lamin B1 loss may be upstream of CCF formation.”
From Cytoplasmic DNA: sources, sensing, and role in aging and disease (2021) · cites this paper as Shimi et al., 2011
Loss of nuclear membrane integrity in senescent cells and laminopathies, such as HGPS, parallels loss of membrane integrity in micronuclei.
“For example, the loss of nuclear membrane integrity in senescent cells (Shimi et al., 2011) and laminopathies, such as HGPS, parallels loss of membrane integrity in MN (Bartsch et al., 2017; Gekara, 2017; Harding et al., 2017; Mackenzie et al., 2017).”
From Cytoplasmic DNA: sources, sensing, and role in aging and disease (2021) · cites this paper as Shimi et al., 2011
SAHF formation is strongly correlated with loss of lamin B1 that allows redistribution and relocation of repressive histone marks from the nuclear periphery into SAHF.
“SAHF formation is strongly correlated with the loss of lamin B1 [279,280,281] that allows the redistribution and relocation of repressive histone marks from the nuclear periphery into SAHF.”
From Mechanisms and Regulation of Cellular Senescence (2021) · cites this paper as [280]
Reduced lamin B1 levels are observed in many senescence models, and its depletion causes senescence.
“Reduced lamin B1 levels are observed in many senescence models, and its depletion causes senescence [279,280,281].”
From Mechanisms and Regulation of Cellular Senescence (2021) · cites this paper as [280]
E2f2 and Lmnb1 are typically downregulated in senescent cells.
“To note, E2f2 and Lmnb1 are typically downregulated in senescent cells [43].”
From The heterogeneity of cellular senescence: insights at the single-cell level (2023) · cites this paper as [43]
A combination of other senescence markers, including p21 induction, Lamin B1 reduction, and 53BP1 foci formation, was used throughout the study.
“we decided to use a combination of other senescence markers, such as the induction of p21Waf1/Cip1/Sdi1 expression28, the reduction of Lamin B1 expression29,30, and the increase of DNA damage response (DDR) marker, such as 53BP1 foci formation27, throughout this study.”
From A BET family protein degrader provokes senolysis by targeting NHEJ and autophagy in senescent cells (2020) · cites this paper as [30]
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Transformation by the human adenoviruses.
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López-Otín, C., Blasco, M. A., Partridge, L., Serrano, M., & Kroemer, G. (2013) · Cell · doi:10.1016/j.cell.2013.05.039 · Cited by 14,982 · see citing works
Cellular Senescence: Defining a Path Forward
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Aging, Cellular Senescence, and Cancer
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Cellular senescence: from physiology to pathology
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The role of senescent cells in ageing
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Cellular senescence in ageing: from mechanisms to therapeutic opportunities
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Cytoplasmic chromatin triggers inflammation in senescence and cancer
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Cellular Senescence: Aging, Cancer, and Injury
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Lamin B1 loss is a senescence-associated biomarker
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Epigenetic mechanisms of longevity and aging
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Cellular senescence and its effector programs
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Autophagy mediates degradation of nuclear lamina
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Self-citationThe dynamic nature of senescence in cancer
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Lysosome-mediated processing of chromatin in senescence
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Orchestrated Intron Retention Regulates Normal Granulocyte Differentiation
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Biomarkers of cellular senescence and skin aging
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Mechanisms and Regulation of Cellular Senescence
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Senescent cells harbour features of the cancer epigenome
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Cell Senescence: Role in Aging and Age-Related Diseases
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Senescent cells: SASPected drivers of age-related pathologies
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The Chromatin Landscape of Cellular Senescence
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Chemically induced reprogramming to reverse cellular aging
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- Authors
- Shimi, T., Butin-Israeli, V., Adam, S. A., Hamanaka, R. B., Goldman, A. E., Lucas, C. A., Shumaker, D. K., Kosak, S. T., Chandel, N. S., & Goldman, R. D.
- Affiliations
- Northwestern University (US)
- ORCID
- Venue
- Genes & Development
- Publisher
- Cold Spring Harbor Laboratory
- Published
- 2011-12-08
- Volume
- 25
- Issue
- 24
- Pages
- 2579-2593
- ISSN
- 0890-9369 (ISSN-L)
- 1549-5477
- PMC
- PMC3248680
- OpenAlex
- W2097265055
- Cited by
- 547
- References
- 98
- Citations by year
- 2026: 23 · 2025: 31 · 2024: 60 · 2023: 53 · 2022: 45 · 2021: 59 · 2020: 39 · 2019: 30 · 2018: 35 · 2017: 22 · 2016: 36 · 2015: 37 · 2014: 35 · 2013: 27 · 2012: 14
- Type
- posted content
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Genes & Development (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Burroughs Wellcome Fund
- Ellison Medical Foundation
- Progeria Research Foundation
- Directorate for Biological Sciences
- National Cancer Institute (R01CA123067, R01CA031760)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nuclear Structure and Function
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Keywords
- cellular senescence, premature senescence, cell proliferation, WI-38 cells, retinoblastoma protein, p53, mitochondrial reactive oxygen species, hypoxia, G1/S cell cycle arrest, oncogenic Ras
- MeSH terms
- Cell Cycle, Cell Line, Cell Nucleus, Cytoskeletal Proteins, Fibroblasts, Gene Expression Regulation, Humans, Signal Transduction, Tumor Suppressor Protein p53, Retinoblastoma Protein, Telomere, Cellular Senescence, Reactive Oxygen Species, ras Proteins, Gene Silencing, Gene Expression Profiling, Cell Proliferation
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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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