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College of Natural Sciences(자연과학대학)Dept. of Chemistry(화학과)CH-Journal Papers(저널논문)

HS-173, a novel phosphatidylinositol 3-kinase (PI3K) inhibitor, has anti-tumor activity through promoting apoptosis and inhibiting angiogenesis

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dc.contributor.authorLee, Hyunseungko
dc.contributor.authorJung, Kyung Heeko
dc.contributor.authorJeong, Yujeongko
dc.contributor.authorHong, Sungwooko
dc.contributor.authorHong, Soon-Sunko
dc.date.accessioned2013-03-12T12:48:51Z-
dc.date.available2013-03-12T12:48:51Z-
dc.date.created2012-12-31-
dc.date.created2012-12-31-
dc.date.issued2013-01-
dc.identifier.citationCANCER LETTERS, v.328, no.1, pp.152 - 159-
dc.identifier.issn0304-3835-
dc.identifier.urihttp://hdl.handle.net/10203/102371-
dc.description.abstractWe synthesized a novel imidazopyridine analogue, a PI3K alpha inhibitor HS-173 and investigated anti-cancer capacity in human cancer cells. HS-173 inhibited the PI3K signaling pathway, and showed anti-proliferative effects on cancer cells. Also, HS-173 induced cell cycle arrest at the G(2)/M phase and apoptosis. In addition, HS-173 decreased the expression HIF-1 alpha and VEGF which play an important role in angiogenesis. This effect was confirmed by the suppression of tube formation and migration assay in vitro. Furthermore. HS-173 diminished blood vessel formation in the Matrigel plug assay in mice. Therefore, HS-173 is considered as a novel drug candidate to treat cancer patients. (C) 2012 Elsevier Ireland Ltd. All rights reserved.-
dc.languageEnglish-
dc.publisherELSEVIER IRELAND LTD-
dc.subjectINDUCIBLE FACTOR-I-
dc.subjectSIGNALING PATHWAY-
dc.subjectGROWTH-FACTOR-
dc.subjectKINASE-ACTIVITY-
dc.subjectCANCER-CELLS-
dc.subjectPIK3CA GENE-
dc.subjectTARGET-
dc.subjectVITRO-
dc.subjectVIVO-
dc.subjectAKT-
dc.titleHS-173, a novel phosphatidylinositol 3-kinase (PI3K) inhibitor, has anti-tumor activity through promoting apoptosis and inhibiting angiogenesis-
dc.typeArticle-
dc.identifier.wosid000311661700018-
dc.identifier.scopusid2-s2.0-84868484417-
dc.type.rimsART-
dc.citation.volume328-
dc.citation.issue1-
dc.citation.beginningpage152-
dc.citation.endingpage159-
dc.citation.publicationnameCANCER LETTERS-
dc.identifier.doi10.1016/j.canlet.2012.08.020-
dc.contributor.localauthorHong, Sungwoo-
dc.contributor.nonIdAuthorLee, Hyunseung-
dc.contributor.nonIdAuthorJung, Kyung Hee-
dc.contributor.nonIdAuthorJeong, Yujeong-
dc.contributor.nonIdAuthorHong, Soon-Sun-
dc.type.journalArticleArticle-
dc.subject.keywordAuthorPI3K inhibitor-
dc.subject.keywordAuthorAnti-cancer drug-
dc.subject.keywordAuthorApoptosis-
dc.subject.keywordAuthorAngiogenesis-
dc.subject.keywordPlusINDUCIBLE FACTOR-I-
dc.subject.keywordPlusSIGNALING PATHWAY-
dc.subject.keywordPlusGROWTH-FACTOR-
dc.subject.keywordPlusKINASE-ACTIVITY-
dc.subject.keywordPlusCANCER-CELLS-
dc.subject.keywordPlusPIK3CA GENE-
dc.subject.keywordPlusTARGET-
dc.subject.keywordPlusVITRO-
dc.subject.keywordPlusVIVO-
dc.subject.keywordPlusAKT-
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