Cucurbitacin D Inhibits the Proliferation of HepG2 Cells and Induces Apoptosis by Modulating JAK/STAT3, PI3K/Akt/mTOR and MAPK Signaling Pathways

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dc.authoridUremis, Muhammed Mehdi/0000-0003-2296-2422
dc.authoridBaysar, Ahmet/0000-0002-7017-399X
dc.authoridTürköz, Yusuf/0000-0001-5401-0720
dc.authorwosidDurhan, Merve/JOK-8847-2023
dc.authorwosidTosun, Emir/S-5125-2018
dc.authorwosidUremis, Muhammed Mehdi/HKP-0531-2023
dc.authorwosidBaysar, Ahmet/Q-1190-2018
dc.authorwosidTürköz, Yusuf/ABG-7931-2020
dc.contributor.authorUremis, Muhammed Mehdi
dc.contributor.authorUremis, Nuray
dc.contributor.authorTosun, Emir
dc.contributor.authorDurhan, Merve
dc.contributor.authorCigremis, Yilmaz
dc.contributor.authorBaysar, Ahmet
dc.contributor.authorTurkoz, Yusuf
dc.date.accessioned2024-08-04T20:53:04Z
dc.date.available2024-08-04T20:53:04Z
dc.date.issued2022
dc.departmentİnönü Üniversitesien_US
dc.description.abstractBackground: Cucurbitacin D (CuD) is a natural compound that can be isolated in various plant families, mainly from Ecballium elaterium (L.) A. Rich. (E. elaterium). It is a triterpenoid with a broad spectrum of biological activity, including anti-cancer properties. Hepatocellular carcinoma, the aggressive type of liver cancer, is an important public health problem worldwide. Objective: In the present study, we investigated the anticancer effect of CuD treated at different doses on the HepG2 cell line and the underlying mechanism in vitro. Methods: CuD was isolated from the fruit juice of E. elaterium plant, and quantitative analysis was performed using high-performance liquid chromatography. The cell viability effect of purified CuD was determined by the MTT test, and also cell apoptosis and cell cycle arrest effects were determined by flow cytometry. DNA damage was evaluated with the comet test. Proteins and genes involved in PI3K/AKT/mTOR, MAPK, and JAK2/STAT3 signaling pathways were evaluated by western blot and qRT-PCR. Results: CuD showed both antiproliferative and cytotoxic effects against the HepG2 cell line in a dose and time-dependent manner. It was observed that CuD induced apoptosis and blocked the cell cycle in HepG2 cells. It was observed that the expressions of genes and some proteins that play a key role in PI3K/AKT/mTOR, MAPK, and JAK2/STAT3 cascades were dose-dependently down-regulated and led to activatation of the apoptotic pathway. Conclusion: All these results show promise that CuD may have a therapeutic effect in hepatocellular carcinoma.en_US
dc.description.sponsorshipInonu University Scientific Research Project Units, Malatya, Turkey [TOA-2018-1317]en_US
dc.description.sponsorshipThis study was funded by Inonu University Scientific Research Project Units (Project no: TOA-2018-1317), Malatya, Turkey.en_US
dc.identifier.doi10.2174/1568009622666220623141158
dc.identifier.endpage944en_US
dc.identifier.issn1568-0096
dc.identifier.issn1873-5576
dc.identifier.issue11en_US
dc.identifier.pmid35786188en_US
dc.identifier.scopus2-s2.0-85139918065en_US
dc.identifier.scopusqualityQ2en_US
dc.identifier.startpage931en_US
dc.identifier.urihttps://doi.org/10.2174/1568009622666220623141158
dc.identifier.urihttps://hdl.handle.net/11616/100942
dc.identifier.volume22en_US
dc.identifier.wosWOS:000874489600006en_US
dc.identifier.wosqualityQ3en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherBentham Science Publ Ltden_US
dc.relation.ispartofCurrent Cancer Drug Targetsen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectCucurbitacinen_US
dc.subjectHepG2en_US
dc.subjecthepatocellular carcinomaen_US
dc.subjectapoptosisen_US
dc.subjectPI3Ken_US
dc.subjectAKTen_US
dc.subjectmTORen_US
dc.subjectMAPKen_US
dc.subjectJAK2en_US
dc.subjectSTAT3en_US
dc.titleCucurbitacin D Inhibits the Proliferation of HepG2 Cells and Induces Apoptosis by Modulating JAK/STAT3, PI3K/Akt/mTOR and MAPK Signaling Pathwaysen_US
dc.typeArticleen_US

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