Publication:
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

dc.contributor.authorÇOKER GÜRKAN, AJDA
dc.contributor.authorsYERLİKAYA P. O., Adacan K., KARATUĞ KAÇAR A., ÇOKER GÜRKAN A., Arisan E. D.
dc.date.accessioned2023-01-16T08:33:59Z
dc.date.accessioned2026-01-10T19:25:54Z
dc.date.available2023-01-16T08:33:59Z
dc.date.issued2023-02-01
dc.description.abstract© 2023 Elsevier LtdEpibrassinolide 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.
dc.identifier.citationYERLİKAYA P. O., Adacan K., KARATUĞ KAÇAR A., ÇOKER GÜRKAN A., Arisan E. D., "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", International Journal of Biochemistry and Cell Biology, cilt.155, 2023
dc.identifier.doi10.1016/j.biocel.2022.106360
dc.identifier.issn1357-2725
dc.identifier.urihttps://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=85145723414&origin=inward
dc.identifier.urihttps://hdl.handle.net/11424/285310
dc.identifier.volume155
dc.language.isoeng
dc.relation.ispartofInternational Journal of Biochemistry and Cell Biology
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectTıp
dc.subjectHistoloji-Embriyoloji
dc.subjectYaşam Bilimleri
dc.subjectMoleküler Biyoloji ve Genetik
dc.subjectSitogenetik
dc.subjectSağlık Bilimleri
dc.subjectTemel Tıp Bilimleri
dc.subjectTemel Bilimler
dc.subjectMedicine
dc.subjectHistology and Embryology
dc.subjectLife Sciences
dc.subjectMolecular Biology and Genetics
dc.subjectCytogenetic
dc.subjectHealth Sciences
dc.subjectFundamental Medical Sciences
dc.subjectNatural Sciences
dc.subjectYaşam Bilimleri (LIFE)
dc.subjectHÜCRE BİYOLOJİSİ
dc.subjectBİYOKİMYA VE MOLEKÜLER BİYOLOJİ
dc.subjectLife Sciences (LIFE)
dc.subjectMOLECULAR BIOLOGY & GENETICS
dc.subjectCELL BIOLOGY
dc.subjectBIOCHEMISTRY & MOLECULAR BIOLOGY
dc.subjectBiyokimya
dc.subjectHücre Biyolojisi
dc.subjectBiochemistry
dc.subjectCell Biology
dc.subjectApoptosis
dc.subjectAutophagy
dc.subjectCell cycle
dc.subjectColon cancer
dc.subjectEpibrassinolide
dc.subjectSCID mouse
dc.subjectEpibrassinolide
dc.subjectColon cancer
dc.subjectSCID Mouse
dc.subjectAutophagy
dc.subjectApoptosis
dc.subjectCell cycle
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 vitro
dc.typearticle
dspace.entity.typePublication

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