29 0

Full metadata record

DC FieldValueLanguage
dc.contributor.author남태규-
dc.date.accessioned2019-05-09T07:28:24Z-
dc.date.available2019-05-09T07:28:24Z-
dc.date.issued2017-10-
dc.identifier.citationMOLECULAR CANCER THERAPEUTICS, v. 16, No. 10, Page. 2144-2156en_US
dc.identifier.issn1538-8514-
dc.identifier.issn1535-7163-
dc.identifier.urihttp://mct.aacrjournals.org/content/early/2017/05/23/1535-7163.MCT-16-0915-
dc.identifier.urihttp://repository.hanyang.ac.kr/handle/20.500.11754/103699-
dc.description.abstractNADPH oxidase-derived reactive oxygen species (ROS) potentiate receptor tyrosine kinase (RTK) signaling, resulting in enhanced angiogenesis and tumor growth. In this study, we report that BJ-1301, a hybrid of pyridinol and alpha-tocopherol, exerts anticancer effects by dual inhibition of NADPH oxidase and RTK activities in endothelial and lung cancer cells. BJ-1301 suppresses ROS production by blocking translocation of NADPH oxidase cytosolic subunits to the cell membrane, thereby inhibiting activation. The potency of RTK inhibition by BJ-1301 was lower than that of sunitinib (a multi-RTK inhibitor), but the inhibition of downstream signaling pathways (e.g., ROS generation) and subsequent biological changes (e.g., NOX2 induction) by BJ-1301 was superior. Consistently, BJ-1301 inhibited cisplatin-resistant lung cancer cell proliferation more than sunitinib did. In xenograft chick or mouse tumor models, BJ-1301 inhibited lung tumor growth, to an extent greater than that of sunitinib or cisplatin. Treatments with BJ-1301 induced regression of tumor growth, potentially due to downregulation of autocrine-stimulatory ligands for RTKs, such as TGFa and stem cell factor, in tumor tissues. Taken together, the current study demonstrates that BJ-1301 is a promising anticancer drug for the treatment of lung cancer.en_US
dc.description.sponsorshipThis work was supported by the Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Korean government (MSIP; NRF-2014R1A2A2A01006833 and NRF-2014R1A4A1071040; through J.A. Kim).en_US
dc.language.isoen_USen_US
dc.publisherAMER ASSOC CANCER RESEARCHen_US
dc.subjectENDOTHELIAL GROWTH-FACTORen_US
dc.subjectNADPH OXIDASESen_US
dc.subjectALPHA-TOCOPHEROLen_US
dc.subjectHYDROGEN-PEROXIDEen_US
dc.subjectEPITHELIAL-CELLSen_US
dc.subjectVITAMIN-Een_US
dc.subjectANGIOGENESISen_US
dc.subjectKITen_US
dc.subjectMETAANALYSISen_US
dc.subjectTOCOTRIENOLen_US
dc.titleDual Inhibition of NOX2 and Receptor Tyrosine Kinase by BJ-1301 Enhances Anticancer Therapy Efficacy via Suppression of Autocrine-Stimulatory Factors in Lung Canceren_US
dc.typeArticleen_US
dc.relation.no10-
dc.relation.volume16-
dc.identifier.doi10.1158/1535-7163.MCT-16-0915-
dc.relation.page2144-2156-
dc.relation.journalMOLECULAR CANCER THERAPEUTICS-
dc.contributor.googleauthorGautam, Jaya-
dc.contributor.googleauthorKu, Jin-Mo-
dc.contributor.googleauthorRegmi, Sushil Chandra-
dc.contributor.googleauthorJeong, Hyunyoung-
dc.contributor.googleauthorWang, Ying-
dc.contributor.googleauthorBanskota, Suhrid-
dc.contributor.googleauthorPark, Myo-Hyeon-
dc.contributor.googleauthorNam, Tae-Gyu-
dc.contributor.googleauthorJeong, Byeong-Seon-
dc.contributor.googleauthorKim, Jung-Ae-
dc.relation.code2017007729-
dc.sector.campusE-
dc.sector.daehakCOLLEGE OF PHARMACY[E]-
dc.sector.departmentDEPARTMENT OF PHARMACY-
dc.identifier.pidtnam-
Appears in Collections:
COLLEGE OF PHARMACY[E](약학대학) > PHARMACY(약학과) > Articles
Files in This Item:
There are no files associated with this item.
Export
RIS (EndNote)
XLS (Excel)
XML


qrcode

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.

BROWSE