ArticleNature communications2024
Nuclear lamin A/C phosphorylation by loss of androgen receptor leads to cancer-associated fibroblast activation.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- A TERRA-NONO axis drives fibroblast reprogramming in cancer.Science advances · 2026Article
- Skin wound healing effects of Pectinodesmus javanensis extract through activation of TGF-β/SMAD signaling pathway.Molecular biology reports · 2026Article
- Lamin A/C as a Molecular Link Between Nuclear Organization, Chromatin Dynamics, and Tumor Progression.Cells · 2026Review
- MMP-3 cleavage of Lamin A induces pro-migratory nuclear deformity, nucleophagy, and their autophagic secretion with extracellular vesicles in metastatic cancer.Cell communication and signaling : CCS · 2026Article
- Integrating multiomics to elucidate the role of chromatin remodeling in glioma and the antitumor mechanisms and therapeutic potential of targeting LMNA.Frontiers in immunology · 2026Article
- Cellular senescence in cancer: from mechanism paradoxes to precision therapeutics.Molecular cancer · 2025Review
- Androgen receptor signalling in non-prostatic malignancies: challenges and opportunities.Nature reviews. Cancer · 2025Review
- Mitochondrial stress disassembles nuclear architecture through proteolytic activation of PKCδ and Lamin B1 phosphorylation in neuronal cells: implications for pathogenesis of age-related neurodegenerative diseases.Frontiers in cellular neuroscience · 2025Article
- Dynamic Post-translational Modifications of Nuclear Lamins in Cellular Function and Pathophysiology.Sub-cellular biochemistry · 2025Review
- Regulation of Stromal Cells by Sex Steroid Hormones in the Breast Cancer Microenvironment.Cancers · 2024Review
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9 authors.
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Abstract
Alterations in nuclear structure and function are hallmarks of cancer cells. Little is known about these changes in Cancer-Associated Fibroblasts (CAFs), crucial components of the tumor microenvironment. Loss of the androgen receptor (AR) in human dermal fibroblasts (HDFs), which triggers early steps of CAF activation, leads to nuclear membrane changes and micronuclei formation, independent of cellular senescence. Similar changes occur in established CAFs and are reversed by restoring AR activity. AR associates with nuclear lamin A/C, and its loss causes lamin A/C nucleoplasmic redistribution. AR serves as a bridge between lamin A/C and the protein phosphatase PPP1. Loss of AR decreases lamin-PPP1 association and increases lamin A/C phosphorylation at Ser 301, a characteristic of CAFs. Phosphorylated lamin A/C at Ser 301 binds to the regulatory region of CAF effector genes of the myofibroblast subtype. Expression of a lamin A/C Ser301 phosphomimetic mutant alone can transform normal fibroblasts into tumor-promoting CAFs.
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