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

Narimah A H Hasani, Khalid Bak, Wan Zurinah Wan Ngah

    Research output: Contribution to journalArticle

    3 Citations (Scopus)

    Abstract

    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 Y-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 cc-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 100μM 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.

    Original languageEnglish
    Pages (from-to)601-609
    Number of pages9
    JournalAsian Biomedicine
    Volume5
    Issue number5
    DOIs
    Publication statusPublished - Oct 2011

    Fingerprint

    Tocotrienols
    Tocopherols
    Mitogen-Activated Protein Kinase Kinases
    Cell death
    Cell Death
    Cells
    Apoptosis
    Proteins
    Growth Inhibitors
    Electrophoresis
    Vitamin E
    Uterine Cervical Neoplasms
    Cell Cycle
    Western Blotting
    Cell Proliferation
    Cell Line
    palm oil
    DNA
    Neoplasms

    Keywords

    • γ-tocotrienol
    • Alpha-tocopherol
    • Anti-proliferation
    • Cervical cancer cell line
    • MEK-2 and ERK-2 protein expressions

    ASJC Scopus subject areas

    • Medicine(all)
    • Biochemistry, Genetics and Molecular Biology(all)

    Cite this

    The anti proliferative effect of palm oil γ-tocotrienol involves alterations in MEK-2 and ERK-2 protein expressions in CaSki cells. / Hasani, Narimah A H; Bak, Khalid; Ngah, Wan Zurinah Wan.

    In: Asian Biomedicine, Vol. 5, No. 5, 10.2011, p. 601-609.

    Research output: Contribution to journalArticle

    Hasani, Narimah A H ; Bak, Khalid ; Ngah, Wan Zurinah Wan. / The anti proliferative effect of palm oil γ-tocotrienol involves alterations in MEK-2 and ERK-2 protein expressions in CaSki cells. In: Asian Biomedicine. 2011 ; Vol. 5, No. 5. pp. 601-609.
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    abstract = "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 Y-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 cc-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 100μM 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.",
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    AB - 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 Y-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 cc-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 100μM 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.

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