ArticleOncotarget2015
The ZEB1/miR-200c feedback loop regulates invasion via actin interacting proteins MYLK and TKS5.
Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 66 citations in OpenAlex.
- Zeb1 Is a Determinant of EMT in Human MDA-MB-231 Breast Cancer Cells and M13-MDA231 Tumor Hybrids.International journal of molecular sciences · 2026Article
- EMT and cell cycle control invadopodia and metastasis in breast cancer via Filip1L.Research square · 2026Article
- Role and underlying mechanisms of miR‑200 family in breast cancer (Review).International journal of oncology · 2026Review
- The Role of Actin-Binding Proteins in Breast Cancer Progression.Breast cancer (Dove Medical Press) · 2026Review
- Mechanical observables of cancer invasion: actin, adhesion, and metastatic plasticity.Frontiers in cell and developmental biology · 2026Review
- Differential Effects of Snail-KO in Human Breast Epithelial Cells and Human Breast Epithelial × Human Breast Cancer Hybrids.International journal of molecular sciences · 2025Article
- The Construction of ceRNA Regulatory Network Unraveled Prognostic Biomarkers and Repositioned Drug Candidates for the Management of Pancreatic Ductal Adenocarcinoma.Current issues in molecular biology · 2025Article
- The Expression and Molecular Roles of MAMDC2 in MSS Colorectal Cancer with a High Tumor Stromal Ratio.Biomedicines · 2025Article
- Altered Phenotypes of Breast Epithelial × Breast Cancer Hybrids after ZEB1 Knock-Out.International journal of molecular sciences · 2023Article
- Zeb1 and Tle3 are trans-factors that differentially regulate the expression of myosin heavy chain-embryonic and skeletal muscle differentiation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2023Article
- Migration speed of captured breast cancer subpopulations correlates with metastatic fitness.Journal of cell science · 2023Article
- Glomerular Endothelial Cell-Derived miR-200c Impairs Glomerular Homeostasis by Targeting Podocyte VEGF-A.International journal of molecular sciences · 2022Article
- Identification of AGR2 Gene-Specific Expression Patterns Associated with Epithelial-Mesenchymal Transition.International journal of molecular sciences · 2022Article
- MicroRNA expression profiling of endocrine sensitive and resistant breast cancer cell lines.Biochemistry and biophysics reports · 2022Article
- Revisiting the miR-200 Family: A Clan of Five Siblings with Essential Roles in Development and Disease.Biomolecules · 2022Review
- miR-205-5p Downregulation andInternational journal of molecular sciences · 2021Article
- Dynamic EMT: a multi-tool for tumor progression.The EMBO journal · 2021Review
- PRG2 and AQPEP are misexpressed in fetal membranes in placenta previa and percreta†.Biology of reproduction · 2021Article
- A single-cell atlas of the healthy breast tissues reveals clinically relevant clusters of breast epithelial cells.Cell reports. Medicine · 2021Article
- SNHG3 promotes migration, invasion, and epithelial-mesenchymal transition of breast cancer cells through the miR-186-5p/ZEB1 axis.American journal of translational research · 2021Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epithelial to mesenchymal transition (EMT) is a developmental process which is aberrantly activated during cancer invasion and metastasis. Elevated expression of EMT-inducers like ZEB1 enables tumor cells to detach from the primary tumor and invade into the surrounding tissue. The main antagonist of ZEB1 in controlling EMT is the microRNA-200 family that is reciprocally linked to ZEB1 in a double negative feedback loop. Here, we further elucidate how the ZEB1/miR-200 feedback loop controls invasion of tumor cells. The process of EMT is attended by major changes in the actin cytoskeleton. Via in silico screening of genes encoding for actin interacting proteins, we identified two novel targets of miR-200c - TKS5 and MYLK (MLCK). Co-expression of both genes with ZEB1 was observed in several cancer cell lines as well as in breast cancer patients and correlated with low miR-200c levels. Depletion of TKS5 or MYLK in breast cancer cells reduced their invasive potential and their ability to form invadopodia. Whereas TKS5 is known to be a major component, we could identify MYLK as a novel player in invadopodia formation. In summary, TKS5 and MYLK represent two mediators of invasive behavior of cancer cells that are regulated by the ZEB1/miR-200 feedback loop.
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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.