ArticleScientific reports2014
E-cadherin-downregulation and RECK-upregulation are coupled in the non-malignant epithelial cell line MCF10A but not in multiple carcinoma-derived cell lines.
Article in Scientific reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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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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Who cites it
21 citing papers in PubMed, 25 citations in OpenAlex.
- The Roles of the Membrane-Anchored Glycoprotein RECK in Animal Development, Tumor Suppression, and Beyond.Life (Basel, Switzerland) · 2026Review
- The Use of Schisandrin B to Combat Triple-Negative Breast Cancers by Inhibiting NLRP3-Induced Interleukin-1β Production.Biomolecules · 2024Article
- Self-assembly of tessellated tissue sheets by expansion and collision.Nature communications · 2022Article
- An RNA Polymerase III General Transcription Factor Engages in Cell Type-Specific Chromatin Looping.International journal of molecular sciences · 2022Article
- Suppression of tumor metastasis by a RECK-activating small molecule.Scientific reports · 2022Article
- Tumorigenic mesenchymal clusters are less sensitive to moderate osmotic stresses due to low amounts of junctional E-cadherin.Scientific reports · 2021Article
- Reversion-inducing cysteine-rich protein with Kazal motifs and MT1-MMP promote the formation of robust fibrillin fibers.Journal of cellular physiology · 2021Article
- Article
- No evidence of involvement of E-cadherin in cell fate specification or the segregation of Epi and PrE in mouse blastocysts.PloS one · 2019Article
- Pathway crosstalk enables cells to interpret TGF-β duration.NPJ systems biology and applications · 2018Article
- Corepressor metastasis-associated protein 3 modulates epithelial-to-mesenchymal transition and metastasis.Chinese journal of cancer · 2017Review
- Promoter hypermethylation of the RECK gene is associated with its low expression and poor survival of esophageal squamous cell carcinoma.Oncology letters · 2017Article
- The inhibition of lung cancer cell migration by AhR-regulated autophagy.Scientific reports · 2017Article
- AKT Axis, miR-21, and RECK Play Pivotal Roles in Dihydroartemisinin Killing Malignant Glioma Cells.International journal of molecular sciences · 2017Article
- Transcriptome profiling in oral cavity and esophagus tissues from (S)-N'-nitrosonornicotine-treated rats reveals candidate genes involved in human oral cavity and esophageal carcinogenesis.Molecular carcinogenesis · 2016Article
- Periostin is identified as a putative metastatic marker in breast cancer-derived exosomes.Oncotarget · 2016Article
- The Wnt7's Tale: A story of an orphan who finds her tie to a famous family.Cancer science · 2016Review
- Bioinformatic Studies to Predict MicroRNAs with the Potential of Uncoupling RECK Expression from Epithelial-Mesenchymal Transition in Cancer Cells.Cancer informatics · 2016Article
- Critical roles for murine Reck in the regulation of vascular patterning and stabilization.Scientific reports · 2015Article
- TMPRSS4 facilitates epithelial-mesenchymal transition of hepatocellular carcinoma and is a predictive marker for poor prognosis of patients after curative resection.Scientific reports · 2015Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Expression of a mesenchymal phenotype is often associated with invasive/metastatic behaviors of carcinoma cells. Acquisition of a mesenchymal phenotype by a carcinoma cell is known as epithelial-mesenchymal transition (EMT). The membrane-anchored matrix metalloproteinase-regulator RECK is abundant in normal mesenchymal cells. In aggressive carcinomas, however, RECK expression is often downregulated. This apparent paradox prompted us to clarify the relationship between EMT and RECK. We found that TGFβ-induced E-cadherin downregulation, a hallmark of EMT, is accompanied by RECK-upregulation in a non-tumorigenic epithelial cell line (MCF10A). In contrast, the loss of E-cadherin expression is uncoupled from RECK-upregulation in carcinoma-derived cell lines (MCF7, MDA-MB-231, and A549). When RECK was artificially expressed in A549 cells, it showed little effect on EMT but elevated the level of integrin α5 and attenuated cell proliferation and migration. These findings implicate RECK in the regulation of proliferation and migration of normal epithelial cells after EMT and suggest how the uncoupling between EMT and RECK-upregulation impacts on the fates and behaviors of carcinoma cells.
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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.