Abstract
Farnesiferol C (Far-C) is a coumarin commonly extracted from
Ferula asafetida
and is popularly used as a traditional source of natural remedy. Liver cancer or hepatocellular carcinoma (HCC) has emerged as a major cause behind cancer burden, and limited therapeutic interventions have further aggravated the clinical management of HCC. In the present study, the authors tested the hypothesis that Far-C-instigated oxidative stress resulted in anti-proliferation and apoptosis instigation within human liver cancer HepG2 cells. The observations reported herewith indicated that Far-C exerted considerable cytotoxic effects on HepG2 cells by reducing the cell viability (
p
< 0.001) in a dose-dependent manner. Far-C exposure also resulted in enhanced ROS production (
p
< 0.01) which subsequently led to loss of mitochondrial membrane potential. Far-C-instigated oxidative stress also led to enhanced nuclear fragmentation and condensation as revealed through Hoechst-33342. These molecular changes post-Far-C exposure also incited apoptotic cell death which concomitantly led to significant activation of caspase-3 (
p
< 0.001). Furthermore, Far-C exhibited its competence in altering the expression of genes involved in apoptosis regulation (
Bax
,
Bad
, and
Bcl2
) along with genes exerting regulatory effects on cell cycle (
cyclinD1
) and its progression (
p21
Cip1
and
CDK4
). The evidence thus clearly shows the preclinical efficacy of Far-C against HepG2 cells. However, further mechanistic investigations deciphering the alteration of different pathways post-Far-C exposure will be highly beneficial.