Please use this identifier to cite or link to this item: http://hdl.handle.net/123456789/3131
Full metadata record
DC FieldValueLanguage
dc.contributor.authorKampo, S.-
dc.contributor.authorAhmmed, B.-
dc.contributor.authorZhou, T.-
dc.contributor.authorOwusu, L.-
dc.contributor.authorAnabah, T. W.-
dc.contributor.authorDoudou, N. R.-
dc.contributor.authorKuugbee, E. D.-
dc.contributor.authorCui, Y.-
dc.contributor.authorLu, Z.-
dc.contributor.authorYan, Q.-
dc.contributor.authorWen, Q.-P.-
dc.date.accessioned2021-06-21T14:06:31Z-
dc.date.available2021-06-21T14:06:31Z-
dc.date.issued2019-
dc.identifier.issn2234-943X-
dc.identifier.urihttp://hdl.handle.net/123456789/3131-
dc.description.abstractA scorpion peptide reported to exhibit both analgesic and antitumor activity in animal models may present as an alternative therapeutic agent for breast cancer. We aimed to investigate the effect of Buthus martensii Karsch antitumor-analgesic peptide (BmK AGAP) on breast cancer cell stemness and epithelial-mesenchymal transition (EMT). We treated MCF-7 and MDA-MB-231 cells with different concentrations of rBmK AGAP and observed that rBmK AGAP inhibited cancer cell stemness, epithelial-mesenchymal transition (EMT), migration, and invasion. Analysis by qPCR, ELISA, western blot, immunofluorescence staining, sphere formation, colony assay, transwell migration, and invasion assays demonstrated rBmK AGAP treatment decreased the expressions of Oct4, Sox2, N-cadherin, Snail, and increased the expression of E-cadherin. rBmK AGAP inhibited breast cancer cell stemness, EMT, migration, and invasion by down-regulating PTX3 through NF- κB and Wnt/β-catenin signaling Pathway in vitro and in vivo. Xenograft tumor model confirmed inhibition of tumor growth, stem-like features, and EMT by rBmK AGAP. Thus, rBmK AGAP is a potential therapeutic agent against breast cancer and related pain.en_US
dc.language.isoenen_US
dc.publisherFrontiers Media SAen_US
dc.relation.ispartofseriesVol. 9;Issue 21-
dc.subjectscorpion venom analgesic peptideen_US
dc.subjectrBmK AGAPen_US
dc.subjectstemnessen_US
dc.subjectepithelial-mesenchymal transitionen_US
dc.subjectpentraxin 3en_US
dc.subjectWnt/β-catenin signalingen_US
dc.subjecttranscription factor NF-κBen_US
dc.subjectbreast canceren_US
dc.titleSCORPION VENOM ANALGESIC PEPTIDE, BMK AGAP INHIBITS STEMNESS, AND EPITHELIAL-MESENCHYMAL TRANSITION BY DOWN-REGULATING PTX3 IN BREAST CANCERen_US
dc.typeArticleen_US
Appears in Collections:School of Medicine and Health Sciences



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