Background:
Coconut oil is an edible oil obtained from fresh, mature coconut kernels. Few studies
have reported the anticancer role of coconut oil. The fatty acid component of coconut oil directly targets the
liver by portal circulation and as chylomicron via lymph. However, the anti-cancer activity of coconut oil
against liver cancer cells and oral cancer cells is yet to be tested. The active component of coconut oil, that is
responsible for the anticancer activity is not well understood. In this study, three different coconut oils, Virgin
Coconut Oil (VCO), Processed Coconut Oil (PCO) and Fractionated Coconut Oil (FCO), were used.
Objective:
Based on previous studies, it can be hypothesized that fatty acids in coconut oil may have anticancer
potential and may trigger cell death in cancer cell lines.
Methods:
Each cell line was treated with different concentrations of Virgin Coconut Oil (VCO), Processed
Coconut Oil (PCO) and Fractionated Coconut Oil (FCO). The treated cells were assayed by MTT after 72 hr of
incubation. The fatty acid composition of different coconut oils was analyzed by gas chromatography.
Result:
Different concentrations of coconut oils were used to treat the cells. Interestingly, the anticancer efficacy
of VCO, PCO and FCO was not uniform, rather the efficacy varied from cell line to cell line. Only 20% VCO
showed significant anticancer activity in HepG2 cells in comparison to 80% PCO against the KB cell line. Remarkably,
20% of PCO and 5% of FCO showed potential growth inhibition in the KB cell line as compared to
80% PCO in HepG2 cells. Moreover, there was a difference in the efficacy of VCO, PCO and FCO, which
might be due to their fatty acid composition. Comparing the anticancer efficacy of VCO, PCO and FCO in this
study helped to predict which class of fatty acids and which fatty acid might be associated with the anticancer
activity of VCO.
Conclusion:
This study shows that VCO, PCO and FCO have anticancer efficacy and may be used for the
treatment of cancer, especially liver and oral cancer.
MicroRNA-1179 suppresses the proliferation and enhances vincristine sensitivity of oral cancer cells via induction of apoptosis and modulation of MEK/ERK and PI3K/AKT signalling pathways
