Cucurbitacin I exhibits anticancer efficacy through induction of apoptosis and modulation of JAK/STAT3, MAPK/ERK, and AKT/mTOR signaling pathways in HepG2 cell line

Basit Öğe Kaydı
dc.authoridBaysar, Ahmet/0000-0002-7017-399X
dc.authoridTürköz, Yusuf/0000-0001-5401-0720
dc.authoridUremis, Muhammed Mehdi/0000-0003-2296-2422
dc.authorwosidBaysar, Ahmet/Q-1190-2018
dc.authorwosidTürköz, Yusuf/ABG-7931-2020
dc.authorwosidTosun, Emir/S-5125-2018
dc.authorwosidUremis, Muhammed Mehdi/HKP-0531-2023
dc.contributor.authorUremis, Nuray
dc.contributor.authorUremis, Muhammed Mehdi
dc.contributor.authorCigremis, Yilmaz
dc.contributor.authorTosun, Emir
dc.contributor.authorBaysar, Ahmet
dc.contributor.authorTurkoz, Yusuf
dc.date.accessioned2024-08-04T20:52:13Z
dc.date.available2024-08-04T20:52:13Z
dc.date.issued2022
dc.departmentİnönü Üniversitesien_US
dc.description.abstractHepatocellular carcinoma is a common cancer type, especially among men. Although cucurbitacin I (CuI), widely found in plants belonging to the Ecballium elaterium (E. L) plant family, has been shown to have antitumorigenic properties in many cancer types, its anticancer effect, molecular mechanism, and apoptotic effect mediated by signal pathways on hepatocellular carcinoma have not been fully clarified. In the present study, we investigated the anticancer effect of CuI treated at different doses on the HepG2 cell line and the underlying mechanism in vitro. High-purity CuI was obtained from the E. elaterium plant with the aid of HPLC. The effects of this substance on the viability of cells were studied by the MTT assay. The effects of CuI on cell cycle progression and apoptosis were studied with flow cytometry. DNA breaks were analyzed by the Comet assay method. The proteins and genes involved in the JAK/STAT3, MAPK/ERK, and AKT/mTOR signaling pathways were investigated using Western blot and qRT-PCR, respectively. The results of this study demonstrated that CuI significantly reduced HepG2 cell growth in vitro, induced antiproliferation, and G2/M phase of the cell cycle was interrupted. Practical applications CuI administration was shown to downregulate the levels of proteins in the PI3K/AKT/mTOR, MAPK, and JAK2/STAT3 cascades in HepG2 cells. CuI also reduced the expression of MAPK, STAT3, mTOR, JAK2, and Akt genes in different concentrations. DNA breaks are formed as a result of this effect. CuI, by reducing cell proliferation and promoting apoptosis, was found to have potential as a chemotherapeutic agent of hepatocellular carcinoma.en_US
dc.description.sponsorshipInonu University Scientific Research Project Units [TOA-2018--1317]en_US
dc.description.sponsorshipInonu University Scientific Research Project Units, Grant/Award Number: TOA-2018--1317en_US
dc.identifier.doi10.1111/jfbc.14333
dc.identifier.issn0145-8884
dc.identifier.issn1745-4514
dc.identifier.issue10en_US
dc.identifier.pmid35866877en_US
dc.identifier.scopus2-s2.0-85134626949en_US
dc.identifier.scopusqualityQ1en_US
dc.identifier.urihttps://doi.org/10.1111/jfbc.14333
dc.identifier.urihttps://hdl.handle.net/11616/100798
dc.identifier.volume46en_US
dc.identifier.wosWOS:000829881700001en_US
dc.identifier.wosqualityQ2en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherWiley-Hindawien_US
dc.relation.ispartofJournal of Food Biochemistryen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectapoptosisen_US
dc.subjectcucurbitacin Ien_US
dc.subjecthepatocellular carcinomaen_US
dc.subjectHepG2en_US
dc.subjectJAK2en_US
dc.subjectSTAT3en_US
dc.subjectMAPKen_US
dc.subjectPI3Ken_US
dc.subjectAKTen_US
dc.subjectmTORen_US
dc.titleCucurbitacin I exhibits anticancer efficacy through induction of apoptosis and modulation of JAK/STAT3, MAPK/ERK, and AKT/mTOR signaling pathways in HepG2 cell lineen_US
dc.typeArticleen_US

Dosyalar

Koleksiyon

WoS İndeksli Yayınlar Koleksiyonu
PubMed İndeksli Yayın Koleksiyonu
Scopus İndeksli Yayınlar Koleksiyonu