ArticleScientific reports2016
Dynamics and plasticity of the epithelial to mesenchymal transition induced by miR-200 family inhibition.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Athero-oncology perspective: identifying hub genes for atherosclerosis diagnosis using machine learning.Frontiers in immunology · 2025Article
- Boolean modeling of mechanosensitive epithelial to mesenchymal transition and its reversal.iScience · 2023Article
- FHOD1 is upregulated in gastric cancer and promotes the proliferation and invasion of gastric cancer cells.Oncology letters · 2021Article
- APC regulation of ESRP1 and p120-catenin isoforms in colorectal cancer cells.Molecular biology of the cell · 2021Article
- Fine-tuning the metabolic rewiring and adaptation of translational machinery during an epithelial-mesenchymal transition in breast cancer cells.Cancer & metabolism · 2020Article
- The mir-200 family regulates key pathogenic events in ascending aortas of individuals with bicuspid aortic valves.Journal of internal medicine · 2019Article
- Group I Paks are essential for epithelial- mesenchymal transition in an Apc-driven model of colorectal cancer.Nature communications · 2018Article
- Characterization of a Merkel Cell Polyomavirus-Positive Merkel Cell Carcinoma Cell Line CVG-1.Frontiers in microbiology · 2018Article
- Metformin Inhibits Tumorigenesis and Tumor Growth of Breast Cancer Cells by Upregulating miR-200c but Downregulating AKT2 Expression.Journal of Cancer · 2017Article
- Downregulation of RIKP by miR-200a promotes the invasive ability of esophageal cancer cells by upregulating the expression of LIN28 and MMP-14.International journal of clinical and experimental pathology · 2017Article
Corrections and comments
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Whereas miR-200 family is known to be involved in the epithelial-to-mesenchymal transition (EMT), a crucial biological process observed in normal and pathological contexts, it has been largely unclear how far the functional levels of these tiny RNAs alone can propagate the molecular events to accomplish this process within several days. By developing a potent inhibitor of miR-200 family members (TuD-141/200c), the expression of which is strictly regulatable by the Tet (tetracycline)-On system, we found using a human colorectal cell line, HCT116, that several direct gene target mRNAs (Zeb1/Zeb2, ESRP1, FN1and FHOD1) of miR-200 family were elevated with distinct kinetics. Prompt induction of the transcriptional suppressors, Zeb1/Zeb2 in turn reduced the expression levels of miR-200c/-141 locus, EpCAM, ESRP1 and E-Cad. The loss of ESRP1 subsequently switched the splicing isoforms of CD44 and p120 catenin mRNAs to mesenchymal type. Importantly, within 9 days after the release from the inhibition of miR-200 family, all of the expression changes in the 14 genes observed in this study returned to their original levels in the epithelial cells. This suggests that the inherent epithelial plasticity is supported by a weak retention of key regulatory gene expression in either the epithelial or mesenchymal states through epigenetic regulation.
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