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Role of JNK Activation and Mitochondrial Bax Translocation in Allicin-Induced Apoptosis in Human Ovarian Cancer SKOV3 Cells.

Xu L, Yu J, Zhai D, Zhang D, Shen W, Bai L, Cai Z, Yu C - Evid Based Complement Alternat Med (2014)

Bottom Line: Results.Conclusions.Our data input new insights to the literature of allicin-induced apoptosis.

View Article: PubMed Central - PubMed

Affiliation: Department of Traditional Chinese Gynecology, Changhai Hospital, Second Military Medical University, Shanghai 200433, China.

ABSTRACT
Background. Allicin, the major component of freshly crushed garlic, is one of the most biologically active compounds of garlic; it has been reported to induce apoptosis in cancer cells; however, the mechanism by which allicin exerts its apoptotic effects is not fully understood. The aim of the present study was to further elucidate the apoptotic pathways induced by allicin in the human ovarian cancer cell line SKOV3. Methods. Cell proliferation and apoptosis were measured by cell-counting assay and flow cytometry analysis. Activation of the signaling pathway was screened by human phospho-kinase array analysis, and the activated pathway and its related proteins were further confirmed by western blot analysis. Results. Allicin induced SKOV3 cell apoptosis and JNK phosphorylation in a time- and dose-dependent manner, but these were significantly blocked by SP600125 (an inhibitor of JNK). The findings suggest that JNK phosphorylation is related to the action of allicin on SKOV3 cells. Furthermore, JNK activation induced Bcl-2 family activation, triggered mitochondria-mediated signaling pathways, and led to the translocation of a considerable amount of Bax and cytochrome c release. Conclusions. JNK activation and mitochondrial Bax translocation are involved in allicin-induced apoptosis in SKOV3 cells. Our data input new insights to the literature of allicin-induced apoptosis.

No MeSH data available.


Related in: MedlinePlus

Inhibitory effect of allicin on SKOV3 cell proliferation. SKOV3 cells were treated with various doses of allicin for 24, 48, and 72 h. Cell proliferation was determined using cell-counting assay and expressed as the percentage of the absorbance value obtained without allicin.
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fig1: Inhibitory effect of allicin on SKOV3 cell proliferation. SKOV3 cells were treated with various doses of allicin for 24, 48, and 72 h. Cell proliferation was determined using cell-counting assay and expressed as the percentage of the absorbance value obtained without allicin.

Mentions: The antiproliferative effect of allicin on SKOV3 cells was examined by exposing the cells to different concentrations of allicin for 24, 48, and 72 h. Cell growth was inhibited in a dose- and time-dependent manner (Figure 1). In the presence of 25 μg/mL of allicin, SKOV3 cells exhibited approximately 60% inhibition of proliferation after treatment for 48 h. As such, this concentration and the treatment time were used in the following experiments. Flow cytometry analysis showed that allicin induced apoptosis significantly, which was also significantly blocked by pretreatment with SP600125 (Figure 2); however, SP600125 alone could not inhibit apoptosis.


Role of JNK Activation and Mitochondrial Bax Translocation in Allicin-Induced Apoptosis in Human Ovarian Cancer SKOV3 Cells.

Xu L, Yu J, Zhai D, Zhang D, Shen W, Bai L, Cai Z, Yu C - Evid Based Complement Alternat Med (2014)

Inhibitory effect of allicin on SKOV3 cell proliferation. SKOV3 cells were treated with various doses of allicin for 24, 48, and 72 h. Cell proliferation was determined using cell-counting assay and expressed as the percentage of the absorbance value obtained without allicin.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4109593&req=5

fig1: Inhibitory effect of allicin on SKOV3 cell proliferation. SKOV3 cells were treated with various doses of allicin for 24, 48, and 72 h. Cell proliferation was determined using cell-counting assay and expressed as the percentage of the absorbance value obtained without allicin.
Mentions: The antiproliferative effect of allicin on SKOV3 cells was examined by exposing the cells to different concentrations of allicin for 24, 48, and 72 h. Cell growth was inhibited in a dose- and time-dependent manner (Figure 1). In the presence of 25 μg/mL of allicin, SKOV3 cells exhibited approximately 60% inhibition of proliferation after treatment for 48 h. As such, this concentration and the treatment time were used in the following experiments. Flow cytometry analysis showed that allicin induced apoptosis significantly, which was also significantly blocked by pretreatment with SP600125 (Figure 2); however, SP600125 alone could not inhibit apoptosis.

Bottom Line: Results.Conclusions.Our data input new insights to the literature of allicin-induced apoptosis.

View Article: PubMed Central - PubMed

Affiliation: Department of Traditional Chinese Gynecology, Changhai Hospital, Second Military Medical University, Shanghai 200433, China.

ABSTRACT
Background. Allicin, the major component of freshly crushed garlic, is one of the most biologically active compounds of garlic; it has been reported to induce apoptosis in cancer cells; however, the mechanism by which allicin exerts its apoptotic effects is not fully understood. The aim of the present study was to further elucidate the apoptotic pathways induced by allicin in the human ovarian cancer cell line SKOV3. Methods. Cell proliferation and apoptosis were measured by cell-counting assay and flow cytometry analysis. Activation of the signaling pathway was screened by human phospho-kinase array analysis, and the activated pathway and its related proteins were further confirmed by western blot analysis. Results. Allicin induced SKOV3 cell apoptosis and JNK phosphorylation in a time- and dose-dependent manner, but these were significantly blocked by SP600125 (an inhibitor of JNK). The findings suggest that JNK phosphorylation is related to the action of allicin on SKOV3 cells. Furthermore, JNK activation induced Bcl-2 family activation, triggered mitochondria-mediated signaling pathways, and led to the translocation of a considerable amount of Bax and cytochrome c release. Conclusions. JNK activation and mitochondrial Bax translocation are involved in allicin-induced apoptosis in SKOV3 cells. Our data input new insights to the literature of allicin-induced apoptosis.

No MeSH data available.


Related in: MedlinePlus