Epibrassinolide impaired colon tumor progression and induced autophagy in SCID mouse xenograft model via acting on cell cycle progression without affecting endoplasmic reticulum stress observed in vitro

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dc.authorscopusidKaan Adacan / 57193356195en_US
dc.authorwosidKaan Adacan / CAQ-1283-2022
dc.contributor.authorObakan Yerlikaya, Pınar
dc.contributor.authorAdacan, Kaan
dc.contributor.authorKaratuğ Kaçar, Ayşe
dc.contributor.authorÇöker Gürkan, Ajda
dc.contributor.authorArısan, Elif Damla
dc.date.accessioned2023-01-19T08:19:21Z
dc.date.available2023-01-19T08:19:21Z
dc.date.issued2023en_US
dc.departmentİstinye Üniversitesien_US
dc.departmentMühendislik ve Doğa Bilimleri Fakültesinen_US
dc.description.abstractEpibrassinolide is a member of brassinosteroids with a polyhydroxysteroid structure similar to steroid hormones of vertebrates. It was shown that EBR decreased cell proliferation and induced apoptosis in different colon cancer cell lines without exerting a cytotoxic effect in epithelial fetal human colon cells. This finding highlighted the potential of epibrassinolide in clinical therapeutic setup. In our previous studies, we showed that epibrassinolide was able to induce apoptosis via endoplasmic reticulum stress. Recently, we also showed that endoplasmic reticulum and apoptotic stresses can be prevented via autophagic induction in non-cancerous epithelial or aggressive forms of cancer cells. Therefore, here in this study, we evaluated the anti-tumoral effect of epibrassinolide as well as the autophagy involvement in the aggressive forms of colon cancer cell lines as well as in vivo SCID mouse xenograft colon cancer model for the first time. For this purpose, SCID mouse model was used for subcutaneous injection of colon cancer cells in matrigel formulation. We found that autophagy is induced in both in vitro and in vivo models. Following tumor formation, SCID mice were treated daily with increasing concentrations of epibrassinolide for two weeks. Our findings showed that EBR inhibited the volume and diameter of the tumor in a dose-dependent manner by causing cell cycle arrest. Therefore our data suggest that epibrassinolide exerts a cytostatic effect on the agrressive form of colon cancer model in vivo, without affecting endoplasmic reticulum stress and the induction of autophagy might have role in this effect of epibrassinolide. © 2023 Elsevier Ltden_US
dc.identifier.citationYerlikaya, P. O., Adacan, K., Kacar, A. K., Gurkan, A. C., & Arisan, E. D. (2022). Epibrassinolide impaired colon tumor progression and induced autophagy in SCID mouse xenograft model via acting on cell cycle progression without affecting endoplasmic reticulum stress observed in vitro. The International Journal of Biochemistry & Cell Biology, 106360.en_US
dc.identifier.doi10.1016/j.biocel.2022.106360en_US
dc.identifier.issn1357-2725en_US
dc.identifier.pmid36587800en_US
dc.identifier.scopus2-s2.0-85145723414en_US
dc.identifier.scopusqualityQ2en_US
dc.identifier.urihttp://doi.org/10.1016/j.biocel.2022.106360
dc.identifier.urihttps://hdl.handle.net/20.500.12713/3819
dc.identifier.volume155en_US
dc.identifier.wosWOS:000916094000001en_US
dc.identifier.wosqualityN/Aen_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.institutionauthorAdacan, Kaan
dc.language.isoenen_US
dc.publisherElsevier Ltden_US
dc.relation.ispartofThe International Journal of Biochemistry & Cell Biologyen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectApoptosisen_US
dc.subjectAutophagyen_US
dc.subjectColon Canceren_US
dc.subjectCell Cycleen_US
dc.subjectEpibrassinolideen_US
dc.subjectSCID Mouseen_US
dc.titleEpibrassinolide impaired colon tumor progression and induced autophagy in SCID mouse xenograft model via acting on cell cycle progression without affecting endoplasmic reticulum stress observed in vitroen_US
dc.typeArticleen_US

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