ArticleClinical and experimental nephrology2016
miR-363 induces transdifferentiation of human kidney tubular cells to mesenchymal phenotype.
Article in Clinical and experimental nephrology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
- Targeting HIF-2α in the Tumor Microenvironment: Redefining the Role of HIF-2α for Solid Cancer Therapy.Cancers · 2022Review
- Therapeutic candidates for keloid scars identified by qualitative review of scratch assay research for wound healing.PloS one · 2021Review
- miR-363 Alleviates Detrusor Fibrosis via the TGF-β1/Smad Signaling Pathway by Targeting Col1a2 in Rat Models of STZ-Induced T2DM.Molecular therapy. Nucleic acids · 2020Article
- Article
- Klotho suppresses the renin-angiotensin system in adriamycin nephropathy.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2017Article
- Generation of kidney tubular organoids from human pluripotent stem cells.Scientific reports · 2016Article
- 5-Aza combined with VPA reprograms human T lineage acute leukemia Jurkat cells into B-cell-like cells by epigenetic activation of PAX5.Biotechnology progressArticle
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
backgroundmicroRNAs (miRNAs) are non-coding small RNAs that regulate embryonic development, cell differentiation and pathological processes via interaction with mRNA. Epithelial-mesenchymal transition (EMT) is pathological process that involves in a variety of diseases such as cancer or fibrosis.
methodsIn this study, we identified miR-363 as a potent inducer of EMT by microarray analysis in human kidney tubular cells, and analyzed the function and mechanisms of miR-363.
resultsOverexpression of miR-363 induced mesenchymal phenotypes with loss of epithelial phenotypes in human kidney tubular cells. In addition, in vitro scratch assay demonstrated that miR-363 promotes cell migration of primary culture of human kidney tubular cells. We identified TWIST/canonical WNT pathway as the downstream effecter of miR-363, and inhibition of canonical WNT by small molecule, IWR-1, attenuated EMT induced by miR-363.
conclusionmiR-363 induces transdifferentiation of human kidney tubular cells via upregulation of TWIST/canonical WNT pathway.
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