ArticleScientific reports2018
A proteomic analysis of an in vitro knock-out of miR-200c.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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.
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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
6 citing papers in PubMed, 10 citations in OpenAlex.
- Unraveling the metastasis-preventing effect of miR-200c in vitro and in vivo.Molecular oncology · 2025Article
- Combating Drug Resistance by Exploiting miRNA-200c-Controlled Phase II Detoxification.Cancers · 2022Article
- The promising potential of piperlongumine as an emerging therapeutics for cancer.Exploration of targeted anti-tumor therapy · 2021Review
- Integrative p53, micro-RNA and Cathepsin Protease Co-Regulatory Expression Networks in Cancer.Cancers · 2020Review
- ZEB1/miR-200c/AGR2: A New Regulatory Loop Modulating the Epithelial-Mesenchymal Transition in Lung Adenocarcinomas.Cancers · 2020Article
- Inducible microRNA-200c decreases motility of breast cancer cells and reduces filamin A.PloS one · 2019Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Loss of miR-200c is correlated to advanced cancer-subtypes due to increased EMT and decreased treatment efficacy by chemotherapeutics. As miRNAs regulate a multitude of targets, the analysis of differentially expressed proteins upon a genomic knock-out (KO) is of interest. In this study, we generated a TALENs KO of miR-200c in MCF7 breast cancer cells, excluded its compensation by family-members and evaluated the impact on the proteome by analyzing three individual KO-clones. We identified 26 key proteins and a variety of enrichments in metabolic and cytoskeletal pathways. In six of these targets (AGR2, FLNA/B, ALDH7A1, SCIN, GSTM3) the differential expression was additionally detected at mRNA level. Together, these alterations in protein abundance accounted for the observed biological phenotypes, i.e. increased migration and chemoresistance and altered metabolism, found in the miR-200c-KO clones. These findings provide novel insights into miR-200c and pave the way for further studies.
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Registered trials
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