ArticleBMC medicine2011
Nuclear envelope structural defects cause chromosomal numerical instability and aneuploidy in ovarian cancer.
Article in BMC medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
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Who cites it
58 citing papers in PubMed, 99 citations in OpenAlex.
- Lamin A/C as a Molecular Link Between Nuclear Organization, Chromatin Dynamics, and Tumor Progression.Cells · 2026Review
- Phosphorylation-dependent modulation of the Lamin A/C-EZH2 complex regulates epithelial-mesenchymal plasticity.Nucleic acids research · 2026Article
- Lamins' role in osteosarcoma.Frontiers in cell and developmental biology · 2026Review
- Setting Up to Divide: Nuclear Mechanotransduction in the Regulation of Mitosis.Results and problems in cell differentiation · 2026Review
- Inverse correlation between Lamin A/C and survival in ovarian cancer: implications for predicting responsiveness to taxane-based chemotherapy.Gynecologic oncology reports · 2025Article
- The Persistent Power of the Taxane/Platin Chemotherapy.Cancers · 2025Review
- The Second Selectivity of Taxanes to Malignant Cells --- Nuclear Envelope Malleability.Journal of Cancer · 2025Article
- Emerin expression stratification across breast cancer subtypes.Cancer treatment and research communications · 2025Article
- Cancer nuclear envelope rupture and repair in taxane resistance.Medical review (2021) · 2024Review
- Patterns of Aneuploidy and Signaling Consequences in Cancer.Cancer research · 2024Review
- Emerin deficiency drives MCF7 cells to an invasive phenotype.bioRxiv : the preprint server for biology · 2024Article
- Review
- TPX2 promotes ovarian tumorigenesis by interacting with Lamin A/C and affecting its stability.Cancer medicine · 2023Article
- Article
- Cell death in cancer chemotherapy using taxanes.Frontiers in pharmacology · 2023Article
- Overview of cellular homeostasis-associated nuclear envelope lamins and associated input signals.Frontiers in cell and developmental biology · 2023Review
- Global crotonylome reveals hypoxia-mediated lamin A crotonylation regulated by HDAC6 in liver cancer.Cell death & disease · 2022Article
- Low Intensity Ultrasound as an Antidote to Taxane/Paclitaxel-induced Cytotoxicity.Journal of Cancer · 2022Review
- Role of Lamin A and emerin in maintaining nuclear morphology in different subtypes of ovarian epithelial cancer.Oncology letters · 2022Article
- Nuclear envelope, chromatin organizers, histones, and DNA: The many achilles heels exploited across cancers.Frontiers in cell and developmental biology · 2022Review
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
Abstract
backgroundDespite our substantial understanding of molecular mechanisms and gene mutations involved in cancer, the technical approaches for diagnosis and prognosis of cancer are limited. In routine clinical diagnosis of cancer, the procedure is very basic: nuclear morphology is used as a common assessment of the degree of malignancy, and hence acts as a prognostic and predictive indicator of the disease. Furthermore, though the atypical nuclear morphology of cancer cells is believed to be a consequence of oncogenic signaling, the molecular basis remains unclear. Another common characteristic of human cancer is aneuploidy, but the causes and its role in carcinogenesis are not well established.
methodsWe investigated the expression of the nuclear envelope proteins lamin A/C in ovarian cancer by immunohistochemistry and studied the consequence of lamin A/C suppression using siRNA in primary human ovarian surface epithelial cells in culture. We used immunofluorescence microscopy to analyze nuclear morphology, flow cytometry to analyze cellular DNA content, and fluorescence in situ hybridization to examine cell ploidy of the lamin A/C-suppressed cells.
resultsWe found that nuclear lamina proteins lamin A/C are often absent (47%) in ovarian cancer cells and tissues. Even in lamin A/C-positive ovarian cancer, the expression is heterogeneous within the population of tumor cells. In most cancer cell lines, a significant fraction of the lamin A/C-negative population was observed to intermix with the lamin A/C-positive cells. Down regulation of lamin A/C in non-cancerous primary ovarian surface epithelial cells led to morphological deformation and development of aneuploidy. The aneuploid cells became growth retarded due to a p53-dependent induction of the cell cycle inhibitor p21.
conclusionsWe conclude that the loss of nuclear envelope structural proteins, such as lamin A/C, may underlie two of the hallmarks of cancer--aberrations in nuclear morphology and aneuploidy.
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