抄録
Background: microRNAs (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. Methods: In 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. Results: Overexpression 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. Conclusion: miR-363 induces transdifferentiation of human kidney tubular cells via upregulation of TWIST/canonical WNT pathway.
| 元の言語 | English |
|---|---|
| ジャーナル | Clinical and Experimental Nephrology |
| DOI | |
| 出版物ステータス | Accepted/In press - 2015 9 15 |
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ASJC Scopus subject areas
- Nephrology
- Physiology
- Physiology (medical)
これを引用
miR-363 induces transdifferentiation of human kidney tubular cells to mesenchymal phenotype. / Morizane, Ryuji; Fujii, Shizuka; Monkawa, Toshiaki; Hiratsuka, Ken; Yamaguchi, Shintaro; Honma, Koichiro; Itoh, Hiroshi.
：: Clinical and Experimental Nephrology, 15.09.2015.研究成果: Article
}
TY - JOUR
T1 - miR-363 induces transdifferentiation of human kidney tubular cells to mesenchymal phenotype
AU - Morizane, Ryuji
AU - Fujii, Shizuka
AU - Monkawa, Toshiaki
AU - Hiratsuka, Ken
AU - Yamaguchi, Shintaro
AU - Honma, Koichiro
AU - Itoh, Hiroshi
PY - 2015/9/15
Y1 - 2015/9/15
N2 - Background: microRNAs (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. Methods: In 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. Results: Overexpression 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. Conclusion: miR-363 induces transdifferentiation of human kidney tubular cells via upregulation of TWIST/canonical WNT pathway.
AB - Background: microRNAs (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. Methods: In 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. Results: Overexpression 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. Conclusion: miR-363 induces transdifferentiation of human kidney tubular cells via upregulation of TWIST/canonical WNT pathway.
KW - Cancer
KW - EMT
KW - Fibrosis
KW - Kidney
KW - miR-363
KW - miRNA
UR - http://www.scopus.com/inward/record.url?scp=84941702722&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84941702722&partnerID=8YFLogxK
U2 - 10.1007/s10157-015-1167-2
DO - 10.1007/s10157-015-1167-2
M3 - Article
C2 - 26373846
AN - SCOPUS:84941702722
JO - Clinical and Experimental Nephrology
JF - Clinical and Experimental Nephrology
SN - 1342-1751
ER -