The phytocannabinoids tetrahydrocannabinol (Δ⁹-THC) and cannabidiol (CBD) and the endocannabinoids 2-arachidonoylethanolamine (anandamide) and 2-arachidonoylglycerol (2-AG) exhibit antiproliferative effect on cancer cells derived from diiferent organs, including thyroid, brain, prostate and breast. THC and the endocannabinoids are known agonists at the G-protein coupled receptors (CB1 and CB2), which appear to mediate the antiproliferative effect on some of the cancer cells. CBD’s antiproliferative effect, on the other hand, is mediated via CB receptor-independent mechanism. In this study, I hypothesized that ovarian cancer cell proliferation will be also inhibited by these cannabinoids. I used the SKOV3 adenocarcinoma cancer line, which exhibits both rapid proliferative and highly invasive properties, for my study. The cells were plated at subconfluent density in DMEM-F12 medium containing 10% fetal bovine serum (FBS). After overnight cell attachment to the culture dish, the cells were incubated for 24 hours in serum-free medium. Subsequently, the cells were exposed to various concentrations of the cannabinoids in serum-free medium for 48 hours. Within 24 hours of incubation with phytocannabinoids at approximately 10 µM, both THC and CBD induced apoptosis and swelling of the cells. Incubation of these cells with a DNA-binding fluorescent dye revealed fragmented nuclei. R-1 methanandamide, a metabolically stable analog of the endocannabinoid anandamide, also induced cell death but at a higher concentration (~30 µM). On the other hand, the endocannabinoid 2-AG increased the proliferation of the cells. The observed differential effects of cannabinoids on SKOV3 cell proliferation support my hypothesis in part.