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miR-519d-3p suppresses tumorigenicity and metastasis by inhibiting Bcl-w and HIF-1α in NSCLC

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dc.contributor.authorChoi, Jae Yeon-
dc.contributor.authorSeok, Hyun Jeong-
dc.contributor.authorKim, Rae-Kwon-
dc.contributor.authorChoi, Mi Young-
dc.contributor.authorLee, Su-Jae-
dc.contributor.authorBae, In Hwa-
dc.date.accessioned2024-01-10T03:37:26Z-
dc.date.available2024-01-10T03:37:26Z-
dc.date.issued2021-09-
dc.identifier.issn2372-7705-
dc.identifier.issn2372-7705-
dc.identifier.urihttps://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/194069-
dc.description.abstractBcl-w, a member of the Bcl-2 family, is highly expressed in various solid tumor, including lung cancer, suggesting that it is involved in cancer cell survival and carcinogenesis. Solid cancer-induced hypoxia has been reported to increase angiogenesis, growth factor, gene instability, invasion, and metastasis. Despite many studies on the treatment of non-small cell lung cancer (NSCLC) with a high incidence rate, the survival rate of patients has not improved because the cancer cells acquired resistance to treatment. This study investigated the correlation between Bcl-w expression and hypoxia in tumor malignancy of NSCLC. Meanwhile, microRNAs (miRNAs) are involved in a variety of key signaling mechanisms associated with hypoxia. Therefore, we discovered miR-519d-3p, which inhibits the expression of Bcl-w and hypoxia-inducing factor (HIF)-1α, and found that it reduces hypoxia-induced tumorigenesis. Spearman's correlation analysis showed that the expression levels of miR-519d-3p and Bcl-w/HIF-1α were negatively correlated, respectively. This showed that miR-519d-3p can be used as a diagnostic biomarker and target therapy for NSCLC.-
dc.format.extent12-
dc.language영어-
dc.language.isoENG-
dc.publisherNature Publishing Group-
dc.titlemiR-519d-3p suppresses tumorigenicity and metastasis by inhibiting Bcl-w and HIF-1α in NSCLC-
dc.typeArticle-
dc.publisher.location미국-
dc.identifier.doi10.1016/j.omto.2021.06.015-
dc.identifier.scopusid2-s2.0-85122661170-
dc.identifier.wosid000701676000029-
dc.identifier.bibliographicCitationMolecular Therapy - Oncolytics, v.22, pp 368 - 379-
dc.citation.titleMolecular Therapy - Oncolytics-
dc.citation.volume22-
dc.citation.startPage368-
dc.citation.endPage379-
dc.type.docTypeArticle-
dc.description.isOpenAccessY-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.relation.journalResearchAreaOncology-
dc.relation.journalResearchAreaResearch & Experimental Medicine-
dc.relation.journalWebOfScienceCategoryOncology-
dc.relation.journalWebOfScienceCategoryMedicine, Research & Experimental-
dc.subject.keywordPlusFACTORS MASTER REGULATORS-
dc.subject.keywordPlusGENE-EXPRESSION-
dc.subject.keywordPlusGLIOBLASTOMA-MULTIFORME-
dc.subject.keywordPlusHYPOXIA-
dc.subject.keywordPlusCANCER-
dc.subject.keywordPlusTUMOR-
dc.subject.keywordPlusCELLS-
dc.subject.keywordPlusANGIOGENESIS-
dc.subject.keywordPlusPROLIFERATION-
dc.subject.keywordPlusINVASION-
dc.subject.keywordAuthorBcl-w-
dc.subject.keywordAuthorHIF-1α-
dc.subject.keywordAuthorhypoxia-
dc.subject.keywordAuthormiR-519d-3p-
dc.subject.keywordAuthorNSCLC-
dc.subject.keywordAuthorsolid tumor-
dc.identifier.urlhttps://www.sciencedirect.com/science/article/pii/S2372770521000966?via%3Dihub-
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