Scopus İndeksli Yayınlar Koleksiyonu
Permanent URI for this collectionhttps://hdl.handle.net/20.500.12573/395
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Article Citation - WoS: 16Citation - Scopus: 16Role of AHR, NF-kB and CYP1A1 Crosstalk With the X Protein of Hepatitis B Virus in Hepatocellular Carcinoma Cells(Elsevier, 2023-02) Celik-Turgut, Gurbet; Olmez, Nazmiye; Koc, Tugba; Ozgun-Acar, Ozden; Semiz, Asli; Dodurga, Yavuz; Sen, AlaattinIn this study, it was aimed to elucidate the interaction between aryl hydrocarbon receptor (AHR), nuclear factor -kappa B (NF-kB), and cytochrome P4501A1 (CYP1A1) with hepatitis B virus X protein (HBX) in a human liver cancer cell line (HepG2) transfected with HBX. First, AHR, NF-kB, and CYP1A1 genes were cloned into the appropriate region of the CheckMate mammalian two-hybrid recipient plasmids using a flexi vector system. Renilla and firefly luciferases were quantified using the dual-luciferase reporter assay system to measure the interactions. Secondly, transient transfections of CYP1A1 and NF-kB (RelA) were performed into HBX-positive and HBX-negative HepG2 cells. The mRNA expression of CYP1A1 and NF-kB genes were confirmed with RT-PCR, and cell viability was measured by WST-1. Further verification was assessed by measuring the activity and protein level of CYP1A1. Additionally, CYP1A1/HBX protein-protein interactions were performed with co-immunoprecipitation, which demonstrated no interaction. These results have clearly shown that the NF-kB and AHR genes interact with HBX without involving CYP1A1 and HBX protein-protein interactions. The present study confirms that AHR and NF-kB interaction plays a role in the HBV mechanism mediated via HBX and coordinating the carcinogenic or inflammatory responses; still, the CYP1A1 gene has no effect on this interaction.Conference Object Hepatoselüler Karsinom Oluşumunda Etkili Moleküler Mekanizmaların İn Siliko Yöntemlerle Araştırılması(Institute of Electrical and Electronics Engineers Inc., 2020-09) Doǧan, Refika Sultan; Saka, Samed; Bakir-Güngör, Burcu; Gungor, Burcu BakirHepatocellular carcinoma (HCC) is the most common cause of cancer-related death in the world. The molecular changes in the organism during the development of HCC are not fully understood. The aim of the present study is to contribute to the identification of critical genes and pathways associated with HCC via integrating various bioinformatics methods. In this study, experiments were conducted on gene expression data of 14 HCC tissues and noncancerous control tissues. A total of 1229 genes, which show a statistically significant change between the groups, were identified. Among these, 681 genes were upregulated and 548 genes were downregulated. Via mapping the detected genes into protein protein interaction networks, active subnetwork search, subnetwork topological analysis and functional enrichment analyses were carried out. The interactions between the molecular pathways affected by HCC were also presented. © 2020 Elsevier B.V., All rights reserved.