https://scholars.lib.ntu.edu.tw/handle/123456789/563156
DC 欄位 | 值 | 語言 |
---|---|---|
dc.contributor.author | KUO-TAI HUA | en_US |
dc.contributor.author | Hong J.-B. | en_US |
dc.contributor.author | YI-SHUAN SHEEN | en_US |
dc.contributor.author | Huang H.-Y. | en_US |
dc.contributor.author | Huang Y.-L. | en_US |
dc.contributor.author | JAU-SHIUH CHEN | en_US |
dc.contributor.author | YI-HUA LIAO | en_US |
dc.date.accessioned | 2021-05-27T08:09:50Z | - |
dc.date.available | 2021-05-27T08:09:50Z | - |
dc.date.issued | 2018 | - |
dc.identifier.issn | 0008-5472 | - |
dc.identifier.uri | https://www.scopus.com/inward/record.uri?eid=2-s2.0-85040193100&doi=10.1158%2f0008-5472.CAN-17-1933&partnerID=40&md5=2eaef38ac8988ca8e376acbc653abe0f | - |
dc.identifier.uri | https://scholars.lib.ntu.edu.tw/handle/123456789/563156 | - |
dc.description.abstract | Increasing evidence suggests that there is a unique cell subpopulation in melanoma that can form nonadherent melanospheres in serum-free stem cell medium, mimicking aggressive malignancy. Using melanospheres as a model to investigate progression mechanisms, we found that miR-519d overexpression was sufficient to promote cell proliferation, migration, invasion, and adhesion in vitro and lung metastatic capability in vivo. The cell adhesion receptor EphA4 was determined to be a direct target of miR-519d. Forced expression of EphA4 reversed the effects of miR-519d overexpression, whereas silencing of EphA4 phenocopied the effect of miR-519d. Malignant progression phenotypes were also affected at the level of epithelial-to-mesenchymal transition and the ERK1/2 signaling pathway inversely affected by miR-519d or EphA4 expression. In clinical specimens of metastatic melanoma, we observed significant upregulation of miR-519d and downregulation of EphA4, in the latter case correlated inversely with overall survival. Taken together, our results suggest a significant functional role for miR-519d in determining EphA4 expression and melanoma progression. Significance: These results suggest a significant role for miR-519d in determining expression of a pivotal cell adhesion molecule that may impact risks of malignant progression in many cancers. ? 2018 American Association for Cancer Research | - |
dc.publisher | American Association for Cancer Research Inc. | - |
dc.relation.ispartof | Cancer Research | - |
dc.subject.classification | [SDGs]SDG3 | - |
dc.subject.other | cisplatin; ephrin receptor A4; microRNA; microRNA 519d; mitogen activated protein kinase 1; mitogen activated protein kinase 3; unclassified drug; ephrin receptor A4; microRNA; MIRN519 microRNA, human; animal cell; animal experiment; animal model; animal tissue; Article; cancer growth; cancer survival; carcinogenesis; cell adhesion; chemosensitivity; concentration (parameters); controlled study; correlational study; cytotoxicity; down regulation; EphA4 gene; epithelial mesenchymal transition; gene function; gene overexpression; gene silencing; human; human cell; human tissue; in vitro study; in vivo study; lung metastasis; male; MAPK signaling; melanoma; mouse; nonhuman; overall survival; phenotype; priority journal; protein expression; tumor growth; tumor invasion; upregulation; 3' untranslated region; animal; cell motion; cell proliferation; down regulation; drug screening; gene expression regulation; genetics; lung tumor; melanoma; metabolism; pathology; SCID mouse; secondary; tumor cell line; 3' Untranslated Regions; Animals; Cell Line, Tumor; Cell Movement; Cell Proliferation; Down-Regulation; Epithelial-Mesenchymal Transition; Gene Expression Regulation, Neoplastic; Humans; Lung Neoplasms; Male; Melanoma; Mice, SCID; MicroRNAs; Receptor, EphA4; Xenograft Model Antitumor Assays | - |
dc.title | miR-519d promotes melanoma progression by downregulating EphA4 | en_US |
dc.type | journal article | en |
dc.identifier.doi | 10.1158/0008-5472.CAN-17-1933 | - |
dc.identifier.pmid | 29093007 | - |
dc.identifier.scopus | 2-s2.0-85040193100 | - |
dc.relation.pages | 216-229 | - |
dc.relation.journalvolume | 78 | - |
dc.relation.journalissue | 1 | - |
item.openairetype | journal article | - |
item.openairecristype | http://purl.org/coar/resource_type/c_6501 | - |
item.cerifentitytype | Publications | - |
item.fulltext | no fulltext | - |
item.grantfulltext | none | - |
crisitem.author.dept | Toxicology | - |
crisitem.author.dept | Dermatology | - |
crisitem.author.dept | Dermatology-NTUH | - |
crisitem.author.dept | Dermatology-NTUH | - |
crisitem.author.dept | Dermatology | - |
crisitem.author.dept | Dermatology-NTUH | - |
crisitem.author.orcid | 0000-0002-8468-4977 | - |
crisitem.author.orcid | 0000-0002-8743-7496 | - |
crisitem.author.orcid | 0000-0002-5701-0109 | - |
crisitem.author.orcid | 0000-0002-4434-3780 | - |
crisitem.author.parentorg | College of Medicine | - |
crisitem.author.parentorg | College of Medicine | - |
crisitem.author.parentorg | National Taiwan University Hospital | - |
crisitem.author.parentorg | National Taiwan University Hospital | - |
crisitem.author.parentorg | College of Medicine | - |
crisitem.author.parentorg | National Taiwan University Hospital | - |
顯示於: | 毒理學研究所 |
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