ArticleThe Journal of cell biology2006
The activity status of cofilin is directly related to invasion, intravasation, and metastasis of mammary tumors.
Article in The Journal of cell biology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 150 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
150 citing papers in PubMed, 274 citations in OpenAlex.
- Inhibition of LIMK by Cofilin-1 peptidomimetics enhances actin depolymerization and reduces metastasis of non-small cell lung cancer.Oncogenesis · 2026Article
- Mechanical observables of cancer invasion: actin, adhesion, and metastatic plasticity.Frontiers in cell and developmental biology · 2026Review
- Cofilin/RhoA and CREB synergistically promote invasion and migration of polyploid giant cancer cells in colorectal cancer.Journal of Cancer · 2026Article
- Suppression of cofilin-1 promotes invasion in 3D hyaluronic acid matrices by promoting actin-based protrusions.Molecular biology of the cell · 2025Article
- Circular RNA circLIMK1-005 promotes the progression of lung adenocarcinoma by interacting with RPA1 protein to activate CDK4 signaling.Cell death discovery · 2025Article
- Regulation and signaling of the LIM domain kinases.BioEssays : news and reviews in molecular, cellular and developmental biology · 2025Review
- Unraveling the protein kinase C/NDRG1 signaling network in breast cancer.Cell & bioscience · 2024Article
- The role of actin cytoskeleton CFL1 and ADF/cofilin superfamily in inflammatory response.Frontiers in molecular biosciences · 2024Review
- Novel Histopathological Biomarkers in Prostate Cancer: Implications and Perspectives.Biomedicines · 2023Review
- Construction of a prognostic model for lung adenocarcinoma based on membrane-tension-related genes.Journal of thoracic disease · 2023Article
- Cooperative NF-κB and Notch1 signaling promotes macrophage-mediated MenaINV expression in breast cancer.Breast cancer research : BCR · 2023Article
- 3,5,3'-Triiodo-L-Thyronine Regulates Actin Cytoskeleton Dynamic in The Differentiated PC-12 Cells during Hypoxia through An αvβ3 Integrin.Cell journal · 2023Article
- Contribution of mechanical homeostasis to epithelial-mesenchymal transition.Cellular oncology (Dordrecht, Netherlands) · 2022Review
- The phosphorylation level of Cofilin-1 is related to the pathological subtypes of gastric cancer.Medicine · 2022Article
- Docetaxel Resistance in Castration-Resistant Prostate Cancer: Transcriptomic Determinants and the Effect of Inhibiting Wnt/β-Catenin Signaling by XAV939.International journal of molecular sciences · 2022Article
- Hydrogen peroxide initiates oxidative stress and proteomic alterations in meningothelial cells.Scientific reports · 2022Article
- Platelet-Derived miR-126-3p Directly Targets AKT2 and Exerts Anti-Tumor Effects in Breast Cancer Cells: Further Insights in Platelet-Cancer Interplay.International journal of molecular sciences · 2022Article
- Cofilin-1 as a potential biomarker forExperimental and therapeutic medicine · 2022Article
- The potential role of cofilin-1 in promoting triple negative breast cancer (TNBC) metastasis via the extracellular vesicles (EVs).Translational oncology · 2022Review
- Overexpression of Mena is associated with tumor progression and poor prognosis in oral squamous cell carcinomaFrontiers in oncology · 2022Article
90 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Understanding the mechanisms controlling cancer cell invasion and metastasis constitutes a fundamental step in setting new strategies for diagnosis, prognosis, and therapy of metastatic cancers. LIM kinase1 (LIMK1) is a member of a novel class of serine-threonine protein kinases. Cofilin, a LIMK1 substrate, is essential for the regulation of actin polymerization and depolymerization during cell migration. Previous studies have made opposite conclusions as to the role of LIMK1 in tumor cell motility and metastasis, claiming either an increase or decrease in cell motility and metastasis as a result of LIMK1 over expression (Zebda, N., O. Bernard, M. Bailly, S. Welti, D.S. Lawrence, and J.S. Condeelis. 2000. J. Cell Biol. 151:1119-1128; Davila, M., A.R. Frost, W.E. Grizzle, and R. Chakrabarti. 2003. J. Biol. Chem. 278:36868-36875; Yoshioka, K., V. Foletta, O. Bernard, and K. Itoh. 2003. Proc. Natl. Acad. Sci. USA. 100:7247-7252; Nishita, M., C. Tomizawa, M. Yamamoto, Y. Horita, K. Ohashi, and K. Mizuno. 2005. J. Cell Biol. 171:349-359). We resolve this paradox by showing that the effects of LIMK1 expression on migration, intravasation, and metastasis of cancer cells can be most simply explained by its regulation of the output of the cofilin pathway. LIMK1-mediated decreases or increases in the activity of the cofilin pathway are shown to cause proportional decreases or increases in motility, intravasation, and metastasis of tumor cells.
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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.