ArticleMolecular biology of the cell2004
A critical role of tropomyosins in TGF-beta regulation of the actin cytoskeleton and cell motility in epithelial cells.
Article in Molecular biology of the cell, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.
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Who cites it
63 citing papers in PubMed, 144 citations in OpenAlex.
- Article
- Tropomyosin Isoforms as Biomarkers for Urothelial Bladder Cancer: Promise and Challenges.Cureus · 2025Review
- Tropomyosin 1 deficiency facilitates cell state transitions and enhances hemogenic endothelial cell specification during hematopoiesis.Stem cell reports · 2024Article
- Twisted-plywood-like tissue formationPNAS nexus · 2024Article
- Tropomyosin1 isoforms underlie epithelial to mesenchymal plasticity, metastatic dissemination, and resistance to chemotherapy in high-grade serous ovarian cancer.Cell death and differentiation · 2024Article
- Tropomyosin 1 deficiency facilitates cell state transitions to enhance hemogenic endothelial cell specification during hematopoiesis.bioRxiv : the preprint server for biology · 2023Article
- TGF-β1 signalling in Alzheimer's pathology and cytoskeletal reorganization: a specialized Tau perspective.Journal of neuroinflammation · 2023Review
- Characteristics of Whale Müller Glia in Primary and Immortalized Cultures.Frontiers in neuroscience · 2022Article
- Measuring the Effects of Cytokines on the Modification of Pericellular Rheology by Human Mesenchymal Stem Cells.ACS biomaterials science & engineering · 2021Article
- Tropomyosin 2.1 collaborates with fibronectin to promote TGF-βRespiratory research · 2021Article
- Arecoline suppresses epithelial cell viability by upregulating tropomyosin-1 through the transforming growth factor-β/Smad pathway.Pharmaceutical biology · 2020Article
- Tropomyosin 3.1 Association With Actin Stress Fibers is Required for Lens Epithelial to Mesenchymal Transition.Investigative ophthalmology & visual science · 2020Article
- miR-21 Overexpression Promotes Esophageal Squamous Cell Carcinoma Invasion and Migration by Repressing Tropomyosin 1.Gastroenterology research and practice · 2020Article
- miRNA‑183‑5p.1 promotes the migration and invasion of gastric cancer AGS cells by targeting TPM1.Oncology reports · 2019Article
- Special Issue on Molecular Research Efforts in Urothelial Carcinoma: Summary of Included Topics.International journal of molecular sciences · 2019Article
- Tropomyosins: Potential Biomarkers for Urothelial Bladder Cancer.International journal of molecular sciences · 2019Review
- Genetic status of KRAS influences Transforming Growth Factor-beta (TGF-β) signaling: An insight into Neuropilin-1 (NRP1) mediated tumorigenesis.Seminars in cancer biology · 2019Review
- High Expression Levels ofJournal of Cancer · 2019Article
- Roles of TGF β and FGF Signals in the Lens: Tropomyosin Regulation for Posterior Capsule Opacity.International journal of molecular sciences · 2018Review
- TGF-β signaling promotes tumor vasculature by enhancing the pericyte-endothelium association.BMC cancer · 2018Article
3 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 5 institutions in 2 countries.
Funding
Abstract
We have investigated transforming growth factor beta (TGF-beta)-mediated induction of actin stress fibers in normal and metastatic epithelial cells. We found that stress fiber formation requires de novo protein synthesis, p38Mapk and Smad signaling. We show that TGF-beta via Smad and p38Mapk up-regulates expression of actin-binding proteins including high-molecular-weight tropomyosins, alpha-actinin and calponin h2. We demonstrate that, among these proteins, tropomyosins are both necessary and sufficient for TGF-beta induction of stress fibers. Silencing of tropomyosins with short interfering RNAs (siRNAs) blocks stress fiber assembly, whereas ectopic expression of tropomyosins results in stress fibers. Ectopic-expression and siRNA experiments show that Smads mediate induction of tropomyosins and stress fibers. Interestingly, TGF-beta induction of stress fibers was not accompanied by changes in the levels of cofilin phosphorylation. TGF-beta induction of tropomyosins and stress fibers are significantly inhibited by Ras-ERK signaling in metastatic breast cancer cells. Inhibition of the Ras-ERK pathway restores TGF-beta induction of tropomyosins and stress fibers and thereby reduces cell motility. These results suggest that induction of tropomyosins and stress fibers play an essential role in TGF-beta control of cell motility, and the loss of this TGF-beta response is a critical step in the acquisition of metastatic phenotype by tumor cells.
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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.