The anti proliferative effect of palm oil γ-tocotrienol involves alterations in MEK-2 and ERK-2 protein expressions in CaSki cells

Background: Vitamin E is a potent growth inhibitor of various cancer cell types in vitro and in vivo. The cell death mechanism is believed to be via cell cycle blockage, differentiation, and apoptosis.

Objectives: To determine the possible involvement of protein expression of MEK-2 and ERK-2 in the cell death mechanism induced by palm oil γ-tocotrienol and α-tocopherol in human cervical cancer cell line, CaSki cells.

Methods: In this study, we tested the effect of γ-tocotrienol and α-tocopherol on the proliferation and apoptosis in CaSki cells. Western blot analysis was used to determine the involvement of MEK-2 and ERK-2 in regulating the cell death mechanism.

Results: Gamma-tocotrienol and α-tocopherol efficiently inhibited the proliferation of CaSki cells by 85.2% to 90.8% (p<0.01, n=4) and 10.2% to 39.1% (p<0.01, n=4) beginning at 100 μM and 50 μM, respectively. The possible cell death mechanism induced by both compounds may be due to apoptosis as confirmed by the presence of cellular DNA fragments separated by electrophoresis and enhancement of apoptotic activity. Treatment with γ-tocotrienol at 150 μM markedly decreased the protein expression of MEK-2 and ERK-2 at 12 hours and 18 hours. In contrast, treatment with α-tocopherol at 300μM has no effect on both protein expressions.

Conclusion: The transient decreases in the protein expression of MEK-2 and ERK-2 suggested that the anti proliferative effect of γ-tocotrienol might involve alteration of the proliferative signaling cascade.