ArticleAmerican journal of physiology. Cell physiology2015
Lamin A/C deficiency reduces circulating tumor cell resistance to fluid shear stress.
Article in American journal of physiology. Cell physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers.
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Who cites it
78 citing papers in PubMed, 113 citations in OpenAlex.
- Lamin subtype expression in Merkel-cell carcinoma: its relation to polyomavirus infection and tumor metastasis.Histochemistry and cell biology · 2026Article
- Mechanoadaptation via Myosin Cytoplasmic Redistribution Protects Circulating Tumor Cells From Shear-induced Death During Hematogenous Dissemination.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Nuclear Mechanotransduction Across the Metastatic Cascade: Decoding Spatiotemporal Heterogeneity in Cancer Dissemination.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Lamin A/C as a Molecular Link Between Nuclear Organization, Chromatin Dynamics, and Tumor Progression.Cells · 2026Review
- Variable A-type lamin expression in Merkel cell carcinoma cell lines and its association with nuclear integrity.Scientific reports · 2026Article
- Review
- Ezrin Functions as a Key Mechanosensitive Effector to Preserve Cell Structure and Promote Survival and Metastasis of Lung Cancer Cells during Circulation.International journal of biological sciences · 2026Article
- Biophysical adaptations of circulating tumor cells undergoing metastasis.Biophysics reports · 2025Article
- Natural medicines target tumor vascular microenvironment to inhibit tumor.Genes & diseases · 2025Review
- Lamin A/C as a biomarker for breast cancer.Molecular biology reports · 2025Review
- The inner nuclear membrane protein, Banf1, has an essential role in triple negative breast cancer cell proliferation and survival.Scientific reports · 2025Article
- Targeting cancer cell stiffness and metastasis with clinical therapeutics.Clinical & experimental metastasis · 2025Review
- Piezo1 regulates actin cytoskeleton remodeling to drive EMT in cervical cancer through the RhoA/ROCK1/PIP2 signaling pathway.Discover oncology · 2025Article
- Article
- The Dual Roles of Lamin A/C in Macrophage Mechanotransduction.Cell proliferation · 2025Article
- Review
- Biomechanics in the tumor microenvironment: from biological functions to potential clinical applications.Experimental hematology & oncology · 2025Review
- Nuclear envelope proteins, mechanotransduction, and their contribution to breast cancer progression.npj biological physics and mechanics · 2025Review
- Advances in research on the relationship between the LMNA gene and human diseases (Review).Molecular medicine reports · 2024Review
- Investigation of the Effect of High Shear Stress on Mesenchymal Stem Cells Using a Rotational Rheometer in a Small-Angle Cone-Plate Configuration.Bioengineering (Basel, Switzerland) · 2024Article
18 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Metastasis contributes to over 90% of cancer-related deaths and is initiated when cancer cells detach from the primary tumor, invade the basement membrane, and enter the circulation as circulating tumor cells (CTCs). While metastasis is viewed as an inefficient process with most CTCs dying within the bloodstream, it is evident that some CTCs are capable of resisting hemodynamic shear forces to form secondary tumors in distant tissues. We hypothesized that nuclear lamins A and C (A/C) act as key structural components within CTCs necessary to resist destruction from elevated shear forces of the bloodstream. Herein, we show that, compared with nonmalignant epithelial cells, tumor cells are resistant to elevated fluid shear forces in vitro that mimic those within the bloodstream, as evidenced by significant decreases in cellular apoptosis and necrosis. Knockdown of lamin A/C significantly reduced tumor cell resistance to fluid shear stress, with significantly increased cell death compared with parental tumor cell and nontargeting controls. Interestingly, lamin A/C knockdown increased shear stress-induced tumor cell apoptosis, but did not significantly affect cellular necrosis. These data demonstrate that lamin A/C is an important structural component that enables tumor cell resistance to fluid shear stress-mediated death in the bloodstream, and may thus facilitate survival and hematogenous metastasis of CTCs.
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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.