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C24H20N2O7, A NOVEL ISONICOTINAMIDE DERIVATIVE, REGULATES THE PROLIFERATION AND APOPTOSIS OF HepG2 CELLS THROUGH REGULATION OF AUTOPHAGY, ROS PRODUCTION AND THE ER

LING DUAN 1,2, ZHANGPING ZHOU 2, HONGDA LIU 3, ZHUOXUAN LIANG 2, SONG TENG 2, XIAOQIONG HE 2*, QIAN YAO 4

1Department of clinical Nutrition, The First People’s Hospital of Yunnan Province, the Affiliated Hospital of Kunming University of Science and Technology, Kunming, 650032, China
2School of Public Health, Kunming Medical University, Kunming, 650500, China
3School of Nursing, Kunming Medical University, Kunming, 650500, China
4Department of Yunnan Cancer Center, The Third Affiliated Hospital to Kunming Medical University, Kunming, 650100, China

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This study explored the anticancer activity of C24H20N2O7 [(E)-N-(1-(6-acetyl-7,9-dihydroxy-8,9b-dimethyl-1,3-dioxo-3,9b-dihydrodibenzo [b,D]furan-2(1-h)-alkylene)ethyl)isonicotinamide], a novel chemical compound modified by esterification of C18H17NO6. MTT assays, colony formation assays, and flow cytometry analyses were performed to investigate the effect of C24H20N2O7 on the proliferation and apoptosis of HepG2 cells in vitro. A xenograft model in nude mice using HepG2 cells was established to validate the effects of C24H20N2O7 in vitro. The results revealed that the proliferation inhibition rate and the apoptosis rate of HepG2 cells were significantly increased in vitro compared with the control group. C24H20N2O7 treatment also inhibited the volume and mass of HepG2 cell mouse xenografts in vivo, and the body weight and the primary organ coefficient did not differ significantly from the control group. C24H20N2O7 may exert its effects through regulation of autophagy, reactive oxygen species, and endoplasmic reticulum regulated apoptosis. These results indicated that C24H20N2O7 inhibited the proliferation of HepG2 cells and promoted their apoptosis, whilst exhibiting low toxicity in vitro and in vivo.