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Comparative research of the cytostatic and cytotoxic effect of the administration of licochalcone A and sorafenib on normal and neoplastic hepatocytes in vitro (Master thesis)

Τάτση, Βησσαρία/ Tatsi, Vissaria

Purpose: The effect of licochalcone A (LCA), a plant phenol, and sorafenib (SOR) co-administration in liver cancer in vitro. Material and Method: The study was performed on normal murine hepatocytes NCTC 1469 and human liver cancer cell line HepG2. Cell viability and growth were assessed by the SRB assay and cytotoxicity by the LDH assay. Results: Cell viability was significantly affected in HepG2 cells after exposure to SOR for 48h. Single administration of LCA generally showed a decrease in cell viability in both cell lines. All combined administrations caused a more intense decrease in the viability of NCTC 1469 cells than the corresponding or higher concentrations of SOR monotherapies, while in HepG2 cells, they exhibited a more intense effect mainly compared to the individual administrations of 5 and 7.5µM SOR. Monotherapies with LCA or SOR generally demonstrated cytostatic activity in both cell lines, but they exhibited a stronger cytotoxic activity in HepG2 cells. All combined administrations demonstrated cytostaticity and caused irreversible damage in the reproductive capacity of HepG2 cells, unlike the respective SOR monotherapies. 20μM LCA enhanced the cytostatic and cytotoxic activity of SOR, particularly in HepG2 cancer cells, to levels similar or greater than monotherapy with 10μM SOR, a concentration higher than those used in the combined administrations. In NCTC 1469 cells, not only did the combined administrations not cause a greater degree of severe damage in cellular functions than all SOR monotherapies, but they also positively affected the cell proliferation rate after substance removal. Conclusions: The combined administration of SOR and LCA seems to be more effective than the single administration of sorafenib in hepatocellular carcinoma, while at the same time the cytoselective effect of LCA is highlighted. Further research is necessary to elucidate the mechanism of action of LCA in normal and cancer cells.