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microRNA-30a arbitrates intestinal-type early gastric carcinogenesis by directly targeting ITGA2

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dc.contributor.authorMin, Jimin-
dc.contributor.authorHan, Tae-Su-
dc.contributor.authorSohn, Yoojin-
dc.contributor.authorShimizu, Takahiro-
dc.contributor.authorChoi, Boram-
dc.contributor.authorBae, Seong-Woo-
dc.contributor.authorHur, Keun-
dc.contributor.authorKong, Seong-Ho-
dc.contributor.authorSuh, Yun-Suhk-
dc.contributor.authorLee, Hyuk-Joon-
dc.contributor.authorKim, Jang-Seong-
dc.contributor.authorMin, Jeong-Ki-
dc.contributor.authorKim, Woo-Ho-
dc.contributor.authorKim, V. Narry-
dc.contributor.authorChoi, Eunyoung-
dc.contributor.authorGoldenring, James R.-
dc.contributor.authorYang, Han-Kwang-
dc.date.accessioned2022-04-15T07:59:41Z-
dc.date.available2022-04-15T07:59:41Z-
dc.date.created2021-01-25-
dc.date.created2021-01-25-
dc.date.created2021-01-25-
dc.date.created2021-01-25-
dc.date.issued2020-07-
dc.identifier.citationGastric Cancer, Vol.23 No.4, pp.600-613-
dc.identifier.issn1436-3291-
dc.identifier.other121481-
dc.identifier.urihttps://hdl.handle.net/10371/178040-
dc.description.abstractBackground Spasmolytic polypeptide-expressing metaplasia (SPEM) is considered a precursor lesion of intestinal metaplasia and intestinal-type gastric cancer (GC), but little is known about microRNA alterations during metaplasia and GC developments. Here, we investigate miR-30a expression in gastric lesions and identify its novel target gene which is associated with the intestinal-type GC. Methods We conducted in situ hybridization and qRT-PCR to determine miR-30a expression in gastric tissues. miR-30a functions were determined through induction or inhibition of miR-30a in GC cell lines. A gene microarray was utilized to confirm miR-30a target genes in GC, and siRNA-mediated target gene suppression and immunostaining were performed. The Cancer Genome Atlas data were utilized to validate gene expressions. Results We found down-regulation of miR-30a during chief cell transdifferentiation into SPEM. MiR-30a level was also reduced in the early stage of GC, and its level was maintained in advanced GC. We identified a novel target gene of miR-30a and ITGA2, and our results showed that either ectopic expression of miR-30a or ITGA2 knockdown suppressed GC cell proliferation, migration, and tumorigenesis. Levels of ITGA2 inversely correlated with levels of miR-30a in human intestinal-type GC. Conclusion We found down-regulation of miR-30a in preneoplastic lesions and its tumor-suppressive functions by targeting ITGA2 in GC. The level of ITGA2, which functions as an oncogene, was up-regulated in human GC. The results of this study suggest that coordination of the miR-30a-ITGA2 axis may serve as an important mechanism in the development of gastric precancerous lesions and intestinal-type GC.-
dc.language영어-
dc.publisherSpringer Verlag-
dc.titlemicroRNA-30a arbitrates intestinal-type early gastric carcinogenesis by directly targeting ITGA2-
dc.typeArticle-
dc.contributor.AlternativeAuthor김빛내리-
dc.identifier.doi10.1007/s10120-020-01052-w-
dc.citation.journaltitleGastric Cancer-
dc.identifier.wosid000517022900001-
dc.identifier.scopusid2-s2.0-85080988873-
dc.citation.endpage613-
dc.citation.number4-
dc.citation.startpage600-
dc.citation.volume23-
dc.identifier.sci000517022900001-
dc.description.isOpenAccessN-
dc.contributor.affiliatedAuthorLee, Hyuk-Joon-
dc.contributor.affiliatedAuthorKim, Woo-Ho-
dc.contributor.affiliatedAuthorKim, V. Narry-
dc.contributor.affiliatedAuthorYang, Han-Kwang-
dc.type.docTypeArticle-
dc.description.journalClass1-
dc.subject.keywordPlusPOLYPEPTIDE-EXPRESSING METAPLASIA-
dc.subject.keywordPlusDECREASES MULTIDRUG-RESISTANCE-
dc.subject.keywordPlusTO-MESENCHYMAL TRANSITION-
dc.subject.keywordPlusCANCER CELLS-
dc.subject.keywordPlusCOLORECTAL-CANCER-
dc.subject.keywordPlusTUMOR-SUPPRESSOR-
dc.subject.keywordPlusMIR-30A-
dc.subject.keywordPlusGROWTH-
dc.subject.keywordPlusPROMOTES-
dc.subject.keywordPlusINVASION-
dc.subject.keywordAuthormiR-30a-
dc.subject.keywordAuthorITGA2-
dc.subject.keywordAuthorMetaplasia-
dc.subject.keywordAuthorGastric cancer-
dc.subject.keywordAuthorTumor suppressor-
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  • College of Natural Sciences
  • School of Biological Sciences
Research Area Molecular Biology & Genetics

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