DSpace logo

Please use this identifier to cite or link to this item: http://142.54.178.187:9060/xmlui/handle/123456789/13271
Full metadata record
DC FieldValueLanguage
dc.contributor.authorDou, Shaohua-
dc.contributor.authorYang, Chao-
dc.contributor.authorZou, Danfeng-
dc.contributor.authorDa, Wa-
dc.contributor.authorMasood, Muqaddas-
dc.contributor.authorAdlat, Salah-
dc.contributor.authorBaima, Yang-Jin-
dc.contributor.authorNasser, MI-
dc.contributor.authorLi, Bin-
dc.contributor.authorJiang, Nan-
dc.date.accessioned2022-10-19T05:59:50Z-
dc.date.available2022-10-19T05:59:50Z-
dc.date.issued2021-07-20-
dc.identifier.issn1011-601X-
dc.identifier.urihttp://142.54.178.187:9060/xmlui/handle/123456789/13271-
dc.description.abstractIn this research, atractylenolide II (ATR II) on apoptosis, cell cycle cells via ER pathway in breast cancer (MDA-MB-231 and MCF-7) cells are assessed. The effect of ATR II on cell proliferation was detected by MTT assay. Additional flow cytometry, luciferase, the western blot were performed to detect the signaling pathway cytotoxicity of ATR II. We have also carried out autodock measurements to validate our results. Our findings showed ATR II could inhibit breast cancer cell growth by apoptosis mainly through G2/M-phase cell cycle arrest. Besides, the cytotoxicity of ATTR II on breast cancer was also correlated by the regulation of endrogen receptors and promising an anti-inflammatory activity via inhibiting NF-KB signaling pathways. Taking together, ATR II could be a potential anticancer drug for breast cancer.en_US
dc.language.isoenen_US
dc.publisherKarachi: Faculty of Pharmacy & Pharmaceutical Sciecnes, University of Karachien_US
dc.subjectATR IIen_US
dc.subjectapoptosisen_US
dc.subjectER/NF-KBen_US
dc.subjectG2/Men_US
dc.subjectautodocken_US
dc.titleAtractylenolide II induces cell cycle arrest and apoptosis in breast cancer cells through ER pathwayen_US
dc.typeArticleen_US
Appears in Collections:Issue 4

Files in This Item:
File Description SizeFormat 
21-8470.htm130 BHTMLView/Open


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