The possible mechanism of action of palm oil γ-tocotrienol and α-tocopherol on the cervical carcinoma CaSki cell apoptosis

Narimah A H Hasani, Permeen A. Yusoff, B. A K Khalid, A. M T Ghapor, Wan Zurinah Wan Ngah

    Research output: Contribution to journalArticle

    8 Citations (Scopus)

    Abstract

    Alpha-, γ-, δ-tocotrienols and γ-tocopherol have been reported to exhibit anti-proliferation effects in several human cancer cells i.e., breast (estrogen-responsive, MDA-MB-435 and estrogen non-responsive, MCF7) and prostate (androgen-sensitive, LNCaP and androgen-resistant, PC-3) via controlling the signal transduction pathways that resulted in an increase in apoptosis. In this study, we tested the effects of γ-tocotrienol, α-tocopherol and α-tocopherol acetate on the proliferation and apoptosis in human cervical carcinoma CaSki cells. The cells were treated with different doses (0 to 300μM) of γ-tocotrienol, α-tocopherol and α-tocopherol acetate and then the proliferation activity were determined using 5-Bromo-2′-deoxy-uridine (BrdU) detection method. Data obtained show that γ-tocotrienol efficiently inhibited the proliferation activity of CaSki cells by 93.5% to 97.8% (p<0.01, n=4) beginning with a dose of 100μM and above with IC50 value of 75μM, while α-tocopherol inhibited the proliferation activity of CaSki cells at lesser magnitude of 19.7% to 39.4% (p<0.01, n=4) beginning with a dose of 50μM and IC20 value of 300μM. On the contrary, α-tocopherol acetate showed no effect on the cell proliferation. The cells apoptotic activity after treatment with different doses of γ-tocotrienol and α-tocopherol (0 to 500μM) was measured using cellular DNA fragmentation ELISA method. In this assay, treatment with 150μM of γ-tocotrienol and 300μM of α-tocopherol had shown to enhance the maximum apoptotic activity of CaSki cells by 6.8 fold (p<0.01, n=4) and 2.7 fold (p<0.01, n=4), respectively as compared to untreated cultures. At the same doses as above, both compounds induced a 50% (p<0.05, n=4) and 40% (p<0.05, n=4) of nuclear apoptotic morphological changes in CaSki cells, respectively as detected using propidium iodide staining. The mechanism of action involved in γ-tocotrienol and α-tocopherol-induced apoptosis was investigated through Western blot analysis. The exposure of both compounds at 150μM and 300μM, respectively for 0, 1, 2, 3, 4, 5, 6, 12, 18, and 24 hours enhanced the expressions of p53, Bax and Caspase-3, and the activity of Caspase-3. These data suggest that p53, Bax and Caspase-3 are involved in the apoptotic signaling cascade induced by γ-tocotrienol and α-tocopherol.

    Original languageEnglish
    Pages (from-to)194-200
    Number of pages7
    JournalBiomedical Research
    Volume19
    Issue number3
    Publication statusPublished - 2008

    Fingerprint

    Tocotrienols
    Tocopherols
    Apoptosis
    Carcinoma
    alpha-Tocopherol
    Cells
    Caspase 3
    Androgens
    Signal transduction
    palm oil
    Propidium
    Cell proliferation
    DNA Fragmentation
    Bromodeoxyuridine
    Inhibitory Concentration 50
    Prostate
    Assays
    Signal Transduction
    Estrogens
    Breast

    Keywords

    • α-tocopherol
    • γ-tocotrienol
    • CaSki cell apoptosis

    ASJC Scopus subject areas

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

    Cite this

    Hasani, N. A. H., Yusoff, P. A., Khalid, B. A. K., Ghapor, A. M. T., & Wan Ngah, W. Z. (2008). The possible mechanism of action of palm oil γ-tocotrienol and α-tocopherol on the cervical carcinoma CaSki cell apoptosis. Biomedical Research, 19(3), 194-200.

    The possible mechanism of action of palm oil γ-tocotrienol and α-tocopherol on the cervical carcinoma CaSki cell apoptosis. / Hasani, Narimah A H; Yusoff, Permeen A.; Khalid, B. A K; Ghapor, A. M T; Wan Ngah, Wan Zurinah.

    In: Biomedical Research, Vol. 19, No. 3, 2008, p. 194-200.

    Research output: Contribution to journalArticle

    Hasani, NAH, Yusoff, PA, Khalid, BAK, Ghapor, AMT & Wan Ngah, WZ 2008, 'The possible mechanism of action of palm oil γ-tocotrienol and α-tocopherol on the cervical carcinoma CaSki cell apoptosis', Biomedical Research, vol. 19, no. 3, pp. 194-200.
    Hasani, Narimah A H ; Yusoff, Permeen A. ; Khalid, B. A K ; Ghapor, A. M T ; Wan Ngah, Wan Zurinah. / The possible mechanism of action of palm oil γ-tocotrienol and α-tocopherol on the cervical carcinoma CaSki cell apoptosis. In: Biomedical Research. 2008 ; Vol. 19, No. 3. pp. 194-200.
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    T1 - The possible mechanism of action of palm oil γ-tocotrienol and α-tocopherol on the cervical carcinoma CaSki cell apoptosis

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    AU - Yusoff, Permeen A.

    AU - Khalid, B. A K

    AU - Ghapor, A. M T

    AU - Wan Ngah, Wan Zurinah

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    N2 - Alpha-, γ-, δ-tocotrienols and γ-tocopherol have been reported to exhibit anti-proliferation effects in several human cancer cells i.e., breast (estrogen-responsive, MDA-MB-435 and estrogen non-responsive, MCF7) and prostate (androgen-sensitive, LNCaP and androgen-resistant, PC-3) via controlling the signal transduction pathways that resulted in an increase in apoptosis. In this study, we tested the effects of γ-tocotrienol, α-tocopherol and α-tocopherol acetate on the proliferation and apoptosis in human cervical carcinoma CaSki cells. The cells were treated with different doses (0 to 300μM) of γ-tocotrienol, α-tocopherol and α-tocopherol acetate and then the proliferation activity were determined using 5-Bromo-2′-deoxy-uridine (BrdU) detection method. Data obtained show that γ-tocotrienol efficiently inhibited the proliferation activity of CaSki cells by 93.5% to 97.8% (p<0.01, n=4) beginning with a dose of 100μM and above with IC50 value of 75μM, while α-tocopherol inhibited the proliferation activity of CaSki cells at lesser magnitude of 19.7% to 39.4% (p<0.01, n=4) beginning with a dose of 50μM and IC20 value of 300μM. On the contrary, α-tocopherol acetate showed no effect on the cell proliferation. The cells apoptotic activity after treatment with different doses of γ-tocotrienol and α-tocopherol (0 to 500μM) was measured using cellular DNA fragmentation ELISA method. In this assay, treatment with 150μM of γ-tocotrienol and 300μM of α-tocopherol had shown to enhance the maximum apoptotic activity of CaSki cells by 6.8 fold (p<0.01, n=4) and 2.7 fold (p<0.01, n=4), respectively as compared to untreated cultures. At the same doses as above, both compounds induced a 50% (p<0.05, n=4) and 40% (p<0.05, n=4) of nuclear apoptotic morphological changes in CaSki cells, respectively as detected using propidium iodide staining. The mechanism of action involved in γ-tocotrienol and α-tocopherol-induced apoptosis was investigated through Western blot analysis. The exposure of both compounds at 150μM and 300μM, respectively for 0, 1, 2, 3, 4, 5, 6, 12, 18, and 24 hours enhanced the expressions of p53, Bax and Caspase-3, and the activity of Caspase-3. These data suggest that p53, Bax and Caspase-3 are involved in the apoptotic signaling cascade induced by γ-tocotrienol and α-tocopherol.

    AB - Alpha-, γ-, δ-tocotrienols and γ-tocopherol have been reported to exhibit anti-proliferation effects in several human cancer cells i.e., breast (estrogen-responsive, MDA-MB-435 and estrogen non-responsive, MCF7) and prostate (androgen-sensitive, LNCaP and androgen-resistant, PC-3) via controlling the signal transduction pathways that resulted in an increase in apoptosis. In this study, we tested the effects of γ-tocotrienol, α-tocopherol and α-tocopherol acetate on the proliferation and apoptosis in human cervical carcinoma CaSki cells. The cells were treated with different doses (0 to 300μM) of γ-tocotrienol, α-tocopherol and α-tocopherol acetate and then the proliferation activity were determined using 5-Bromo-2′-deoxy-uridine (BrdU) detection method. Data obtained show that γ-tocotrienol efficiently inhibited the proliferation activity of CaSki cells by 93.5% to 97.8% (p<0.01, n=4) beginning with a dose of 100μM and above with IC50 value of 75μM, while α-tocopherol inhibited the proliferation activity of CaSki cells at lesser magnitude of 19.7% to 39.4% (p<0.01, n=4) beginning with a dose of 50μM and IC20 value of 300μM. On the contrary, α-tocopherol acetate showed no effect on the cell proliferation. The cells apoptotic activity after treatment with different doses of γ-tocotrienol and α-tocopherol (0 to 500μM) was measured using cellular DNA fragmentation ELISA method. In this assay, treatment with 150μM of γ-tocotrienol and 300μM of α-tocopherol had shown to enhance the maximum apoptotic activity of CaSki cells by 6.8 fold (p<0.01, n=4) and 2.7 fold (p<0.01, n=4), respectively as compared to untreated cultures. At the same doses as above, both compounds induced a 50% (p<0.05, n=4) and 40% (p<0.05, n=4) of nuclear apoptotic morphological changes in CaSki cells, respectively as detected using propidium iodide staining. The mechanism of action involved in γ-tocotrienol and α-tocopherol-induced apoptosis was investigated through Western blot analysis. The exposure of both compounds at 150μM and 300μM, respectively for 0, 1, 2, 3, 4, 5, 6, 12, 18, and 24 hours enhanced the expressions of p53, Bax and Caspase-3, and the activity of Caspase-3. These data suggest that p53, Bax and Caspase-3 are involved in the apoptotic signaling cascade induced by γ-tocotrienol and α-tocopherol.

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