ArticleCell stress2017
Reciprocal regulatory circuits coordinating EMT plasticity.
Article in Cell stress, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
2 citing papers in PubMed, 2 citations in OpenAlex.
- Review
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epithelial to mesenchymal transition (EMT) as well as its reversal process, mesenchymal to epithelial transition (MET), are essential and well-controlled cellular processes during embryonic development. Tightly controlled regulatory mechanisms guide an EMT/MET plasticity and enable cells to switch forth and back between different cell morphologies and functional capabilities to endow the necessity of tissue plasticity. However, aberrant and uncontrolled activation of these processes during malignant tumor progression promotes primary tumor cell invasion, cancer cell dissemination and metastatic outgrowth. In a recent study (Nat Commun; doi: 10.1038/s41467-017-01197-w), we have reported on the post-transcriptional control of normal and cancer-associated EMT by miRNAs and identified a novel, critical double-negative feedback regulation of the thus far unknown miRNA miR1199 and the key EMT transcription factor Zeb1.
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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.