ArticleCell cycle (Georgetown, Tex.)2015
Mutant lamin A links prophase to a p53 independent senescence program.
Article in Cell cycle (Georgetown, Tex.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
13 citing papers in PubMed, 18 citations in OpenAlex.
- High matrix stiffness promotes senescence of type II alveolar epithelial cells by lysosomal degradation of lamin A/C in pulmonary fibrosis.Respiratory research · 2025Article
- Polyploid giant cancer cells: origin, possible pathways of formation, characteristics, and mechanisms of regulation.Frontiers in cell and developmental biology · 2024Review
- Overview of cellular homeostasis-associated nuclear envelope lamins and associated input signals.Frontiers in cell and developmental biology · 2023Review
- Lamin-A/C Is Modulated by the Involvement of Histamine-Mediated Calcium/Calmodulin-Dependent Kinase II in Lung Cancer Cells.International journal of molecular sciences · 2022Article
- NTRK1/TrkA Signaling in Neuroblastoma Cells Induces Nuclear Reorganization and Intra-Nuclear Aggregation of Lamin A/C.Cancers · 2021Article
- Lamin A/C: Function in Normal and Tumor Cells.Cancers · 2020Review
- Transcriptome signature of ventricular arrhythmia in dilated cardiomyopathy reveals increased fibrosis and activated TP53.Journal of molecular and cellular cardiology · 2020Article
- Inhibition of FAK Signaling Elicits Lamin A/C-Associated Nuclear Deformity and Cellular Senescence.Frontiers in oncology · 2019Article
- Whole Chromosome Instability induces senescence and promotes SASP.Scientific reports · 2016Article
- Tying up loose ends: telomeres, genomic instability and lamins.Current opinion in genetics & development · 2016Review
- Article
- A PTEN inhibitor displays preclinical activity against hepatocarcinoma cells.Cell cycle (Georgetown, Tex.) · 2016Article
- Trapping cells in senescence with a lamin cage.Cell cycle (Georgetown, Tex.) · 2015Article
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Expression of oncogenes or short telomeres can trigger an anticancer response known as cellular senescence activating the p53 and RB tumor suppressor pathways. This mechanism is switched off in most tumor cells by mutations in p53 and RB signaling pathways. Surprisingly, p53 disabled tumor cells could be forced into senescence by expression of a mutant allele of the nuclear envelope protein lamin A. The pro-senescence lamin A mutant contains a deletion in the sequence required for processing by the protease ZMPSTE24 leading to accumulation of farnesylated lamin A in the nuclear envelope. In addition, the serine at position 22, a target for CDK1-dependent phosphorylation, was mutated to alanine, preventing CDK1-catalyzed nuclear envelope disassembly. The accumulation of this mutant lamin A compromised prophase to prometaphase transition leading to invaginations of the nuclear lamina, nuclear fragmentation and impaired chromosome condensation. Cells exited this impaired mitosis without cytokinesis and re-replicated their DNA ultimately arresting in interphase as polyploid cells with features of cellular senescence including increased expression of inflammatory gene products and a significant reduction of tumorigenicity in vivo.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.