289 0

Full metadata record

DC FieldValueLanguage
dc.contributor.author이수재-
dc.date.accessioned2019-05-13T08:21:30Z-
dc.date.available2019-05-13T08:21:30Z-
dc.date.issued2019-02-
dc.identifier.citationINTERNATIONAL JOURNAL OF NANOMEDICINE, Page. 1131-1148en_US
dc.identifier.issn1178-2013-
dc.identifier.urihttps://www.dovepress.com/gold-quantum-dots-impair-the-tumorigenic-potential-of-glioma-stem-like-peer-reviewed-article-IJN-
dc.identifier.urihttps://repository.hanyang.ac.kr/handle/20.500.11754/104083-
dc.description.abstractBackground Over the past several decades, the incidence of solid cancers has rapidly increased worldwide. Successful removal of tumor-initiating cells within tumors is essential in the field of cancer therapeutics to improve patient disease-free survival rates. The biocompatible multivarient-sized gold nanoparticles (MVS-GNPs) from quantum dots (QDs, <10 nm) to nanosized (up to 50 nm) particles have vast applications in various biomedical areas including cancer treatment. The role of MVS-GNPs for inhibition of tumorigenic potential and stemness of glioma was investigated in this study. Methods Herein, MVS-GNPs synthesized and characterized by means of X-ray diffraction pattern (XRD) and transmission electron microscopy (TEM) techniques. Afterwards, interaction of these GNPs with glioma stem-cell like cells along with cancer cells were evaluated by MTT, cell motility, self-renewal assays and biostatistics was also applied. Results Among these GNPs, G-QDs contributed to reduce metastatic events and spheroid cell growth, potentially blocking the self-renewal ability of these cells. This study also uncovers the previously unknown role of the inhibition of CTNNB1 signaling as a novel candidate to decrease the tumorigenesis of glioma spheroids and subsequent spheroid growth. The accurate and precise biostatistics results were obtained at quantify level. Conclusion In summary, G-QDs may exhibit possible contribution on suppressing the growth of tumor-initiating cells. These data reveal a unique therapeutic approach for the elimination of residual resistant stem-like cells during cancer treatment.en_US
dc.description.sponsorshipThis study was financially supported by the King Saud University, Vice Deanship of Research Chairs. This work was supported by a grant from the National Research Foundation of Korea (NRF), which is funded by the Korean Government, Ministry of Science, ICT and Future Planning (MSIP) NRF-2016K1A4A3914113 and NRF-2016R1C1B2010851. This work is also supported by Kwangwoon University Research Grant in 2018–19. This research was also supported by the Bio & Medical Technology Development Program of the NRF funded by MSIP (No-2017M3A9G8084539).en_US
dc.language.isoenen_US
dc.publisherDOVE MEDICAL PRESS LTDen_US
dc.subjectmultivarient gold nanoparticlesen_US
dc.subjectepithelial-mesenchymal transitionen_US
dc.subjectsolid tumoren_US
dc.subjectbrain canceren_US
dc.subjectself-renewalen_US
dc.subjectcellular movementen_US
dc.subjectbiostatisticsen_US
dc.titleGold quantum dots impair the tumorigenic potential of glioma stem-like cells via β-catenin downregulation in vitroen_US
dc.typeArticleen_US
dc.identifier.doi10.2147/IJN.S195333-
dc.relation.page1131-1148-
dc.relation.journalINTERNATIONAL JOURNAL OF NANOMEDICINE-
dc.contributor.googleauthorWahab, Rizwan-
dc.contributor.googleauthorKaushik, Neha-
dc.contributor.googleauthorKhan, Farheen-
dc.contributor.googleauthorKaushik, Nagendra Kumar-
dc.contributor.googleauthorLee, Su-Jae-
dc.contributor.googleauthorChoi, Eun Ha-
dc.contributor.googleauthorAl-Khedhairy, Abdulaziz A-
dc.relation.code2019001001-
dc.sector.campusS-
dc.sector.daehakCOLLEGE OF NATURAL SCIENCES[S]-
dc.sector.departmentDEPARTMENT OF LIFE SCIENCE-
dc.identifier.pidsj0420-
Appears in Collections:
COLLEGE OF NATURAL SCIENCES[S](자연과학대학) > LIFE SCIENCE(생명과학과) > 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