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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

Effect of allicin and/or SP600125 on the phosphorylation of JNK in SKOV3 cells. (a) Treatment with various concentrations of allicin for 15 min. (b) Treatment with 25 μg/mL of allicin at indicated times. (c) Pretreatment with 20 μM SP600125 for 30 min before incubation with 25 μg/mL of allicin for 15 min; JNK phosphorylation was measured by western blot analysis after 48 h.
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fig3: Effect of allicin and/or SP600125 on the phosphorylation of JNK in SKOV3 cells. (a) Treatment with various concentrations of allicin for 15 min. (b) Treatment with 25 μg/mL of allicin at indicated times. (c) Pretreatment with 20 μM SP600125 for 30 min before incubation with 25 μg/mL of allicin for 15 min; JNK phosphorylation was measured by western blot analysis after 48 h.

Mentions: Human phospho-kinase array assays were performed to discover which signaling pathways are involved in allicin-induced SKOV3 cell apoptosis. The AKT and JNK pathways were activated (see supplementary data in Supplementary Material available online at http://dx.doi.org/10.1155/2014/378684). As activation of the JNK pathway is a novel finding in this setting, we focused on it in the following experiments. Phospho-JNK increased in a dose-dependent manner (Figure 3(a)), and peak phosphorylation was detected at 15 min—when the cells were treated with 25 μg/mL of allicin (Figure 3(b)). Furthermore, SP600125 could partially inhibit JNK phosphorylation as activated by allicin (Figure 3(c)), revealing that allicin-induced apoptosis is related to the JNK MAPK signaling pathway in SKOV3 cells.


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)

Effect of allicin and/or SP600125 on the phosphorylation of JNK in SKOV3 cells. (a) Treatment with various concentrations of allicin for 15 min. (b) Treatment with 25 μg/mL of allicin at indicated times. (c) Pretreatment with 20 μM SP600125 for 30 min before incubation with 25 μg/mL of allicin for 15 min; JNK phosphorylation was measured by western blot analysis after 48 h.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

fig3: Effect of allicin and/or SP600125 on the phosphorylation of JNK in SKOV3 cells. (a) Treatment with various concentrations of allicin for 15 min. (b) Treatment with 25 μg/mL of allicin at indicated times. (c) Pretreatment with 20 μM SP600125 for 30 min before incubation with 25 μg/mL of allicin for 15 min; JNK phosphorylation was measured by western blot analysis after 48 h.
Mentions: Human phospho-kinase array assays were performed to discover which signaling pathways are involved in allicin-induced SKOV3 cell apoptosis. The AKT and JNK pathways were activated (see supplementary data in Supplementary Material available online at http://dx.doi.org/10.1155/2014/378684). As activation of the JNK pathway is a novel finding in this setting, we focused on it in the following experiments. Phospho-JNK increased in a dose-dependent manner (Figure 3(a)), and peak phosphorylation was detected at 15 min—when the cells were treated with 25 μg/mL of allicin (Figure 3(b)). Furthermore, SP600125 could partially inhibit JNK phosphorylation as activated by allicin (Figure 3(c)), revealing that allicin-induced apoptosis is related to the JNK MAPK signaling pathway in SKOV3 cells.

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