Anticancer effects of imidazole nucleus in hepatocellular carcinoma cell lines via the inhibition of AKT and ERK1/2 signaling pathways

Basit Öğe Kaydı
dc.authoridKahraman, Erkan/0000-0003-0051-416X
dc.authoridGOKER, ERDEM/0000-0001-6180-713X
dc.authorscopusid57204097891
dc.authorscopusid26662691100
dc.authorwosidKahraman, Erkan/AAE-6696-2019
dc.contributor.authorKahraman, Erkan
dc.contributor.authorGoker, Erdem
dc.date.accessioned2023-01-12T19:50:48Z
dc.date.available2023-01-12T19:50:48Z
dc.date.issued2022
dc.departmentN/A/Departmenten_US
dc.description.abstractBackground Imidazole nucleus has been used efficiently in the development of many drug molecules due to its therapeutic effects. Many derivatives of it have been produced particularly for use in cancer treatment. However, the anti-cancer effects of imidazole nucleus in liver cancer cells are as yet unclear. In this study, we aimed to investigate the anti-cancer effects of imidazole nucleus in hepatocellular carcinoma (HCC) cell lines. Methods and results Anti-cancer effect of imidazole nucleus was investigated using cell viability assay, apoptosis analysis, cell migration analysis, cell morphology analysis, colony formation assay and 3D cell culture techniques in HuH-7 and Mahlavu cell lines. Also, effect of imidazole on AKT and ERK1/2 pathways were determined using by western blot analysis. Imidazole decreased cell viability in both HCC cell lines in a dose and time-dependent manner and also suppressed the colony forming ability of the cells (p < 0.05). Imidazole increased the cleaved caspase 3 protein levels and thus induced apoptosis (p < 0.05). Imidazole induced morphological alterations and autophagy by increasing intracellular vacuolization. Also, imidazole decreased the viability and dimensions of HCC cell tumor spheroids produced in 3D cell cultures (p < 0.05). Moreover, it was observed that all of these effects, are defined above, appeared in parallel with suppression of AKT and ERK1/2 signaling pathways by imidazole nucleus. Conclusions The findings of this present study established the anti-cancer effects of imidazole nucleus in HCC cell lines and showed that it could be a potential molecule in the treatment of HCC via inhibition of AKT and ERK1/2 signaling pathways.en_US
dc.description.sponsorshipAcademic Oncology Association from Turkeyen_US
dc.description.sponsorshipWe would like to thank Academic Oncology Association from Turkey for funding support. We thank Professor Dr. Nee Atabey for providing us with the HCC cell lines.en_US
dc.identifier.doi10.1007/s11033-022-07273-9
dc.identifier.endpage4388en_US
dc.identifier.issn0301-4851
dc.identifier.issn1573-4978
dc.identifier.issue6en_US
dc.identifier.pmid35226260en_US
dc.identifier.scopus2-s2.0-85125539026en_US
dc.identifier.scopusqualityQ2en_US
dc.identifier.startpage4377en_US
dc.identifier.urihttps://doi.org/10.1007/s11033-022-07273-9
dc.identifier.urihttps://hdl.handle.net/11454/76172
dc.identifier.volume49en_US
dc.identifier.wosWOS:000762161700001en_US
dc.identifier.wosqualityQ3en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherSpringeren_US
dc.relation.ispartofMolecular Biology Reportsen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectImidazoleen_US
dc.subjectHepatocellular carcinomaen_US
dc.subjectCanceren_US
dc.subjectCancer drugsen_US
dc.subjectLiver canceren_US
dc.subjectCanceren_US
dc.subjectApoptosisen_US
dc.subjectDerivativesen_US
dc.subjectAutophagyen_US
dc.subjectDnaen_US
dc.subjectActivationen_US
dc.subjectTargetsen_US
dc.subjectBindingen_US
dc.titleAnticancer effects of imidazole nucleus in hepatocellular carcinoma cell lines via the inhibition of AKT and ERK1/2 signaling pathwaysen_US
dc.typeArticleen_US

Dosyalar

Koleksiyon

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