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6. Uluslararası ve 35. Ulusal Biyofizik Kongresi , Kayseri, Turkey, 4 - 06 September 2024, pp.1, (Summary Text)
Aim: Hepatocellular carcinoma is a fatal with a significant incidence worldwide. It is important to investigate biomarkers and new treatment approaches in order to diagnose the disease in its early stages. Anomalies in glucose play an important role in tumor development and progression. Aerobic glycolysis increases in cancer cells due to the Warburg effect. Glucose transport across the cell membrane becomes important at this stage. Increased GLUT1 expression has been associated with poor prognosis in various cancers. In our study, a steatosis cell model was created. It was aimed to examine the mechanism of action of BAY-876 on lactate, ATP levels and the apoptosis signal transduction in the HepG2 and steatosis HepG2 cells. Methods: Studies were conducted when cell viability was higher than 95%. Confirmation of the lubrication pattern was done by Oil red-O staining. Lactate and ATP analysis kits were used during the experiments. Caspase 3, Bcl-2/Bax and cytochrome c were examined using the western blot technique. Mann-Whitney, one-way or two-way ANOVA variance tests were used. Results: Both cells treated with BAY-876, inhibition of lactate (p˂0.01) and ATP level (p˂0.05) was found to be significant compared to the control . A significant increase in cytochrome c, caspase 3 and Bax/Bcl-2 levels was detected in the BAY-876-treated group in HepG2 cells compared to the control groups (p˂0.0001). Cytochrome c and Bax/Bcl-2 levels in steatosis HepG2 cells increased compared to the control group (p˂0.001). In HepG2 cells, a significant decrease in cytochrome c and an increase in Bax/Bcl-2 levels were detected compared to steatosis HepG2 cells (p˂0.01).
Conclusions: BAY-876 caused inhibition of lactate and ATP levels. Apoptosis proteins increased in both cells. It is anticipated that our study will contribute to the literature, BAY876 anticancer drug research studies, and elucidation of the signal transduction mechanism of hepatocellular carcinoma.
Key Words: BAY-876, hepatocellular carcinoma, steatosis, apoptosis.
Acknowledgments: This work was supported by the title "Studies on the investigation of the anticancer effects of the glucose transporter 1 inhibitor BAY-876 in HepG2 cells and steatosis cell model in hepatocellular carcinoma" by Marmara University BAP Commission with project number SAG-C-DRP-TDK-2021-10286 and TUBITAK 1002 with project number SBAG-221S561.