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Apoptotic effect of cordycepin combined with cisplatin and/or paclitaxel on MA-10 mouse Leydig tumor cells.

Kang FC, Chen PJ, Pan BS, Lai MS, Chen YC, Huang BM - Onco Targets Ther (2015)

Bottom Line: Cell cycle analysis showed that combination treatment significantly increased subG1 phase cell numbers in MA-10 cells, indicating apoptosis.Moreover, cordycepin plus cisplatin and/or paclitaxel significantly induced cleavage of caspase-8, caspase-9, caspase-3, and poly ADP-ribose polymerase, and phosphorylation of c-Jun NH2-terminal kinase, extracellular signal-regulated kinase, p38, and p53 proteins in MA-10 cells.Cordycepin plus cisplatin and/or paclitaxel can have an additive effect on apoptosis in MA-10 cells, with activation of caspase, mitogen-activated protein kinase, and p53 signal pathways.

View Article: PubMed Central - PubMed

Affiliation: Department of Anesthesia, Chi Mei Medical Center, Chiali, Republic of China.

ABSTRACT

Background: Chemotherapy is not limited to a single treatment, and the evidence demonstrates that different drug combinations can have positive results in patients. In this study, we sought to determine whether cordycepin combined with cisplatin and/or paclitaxel would have an additive effective on inducing apoptosis in mouse Leydig tumor cells, and the mechanisms were also briefly examined.

Methods: The additive effects of cordycepin combined with cisplatin and/or paclitaxel on apoptosis in MA-10 cells were investigated by monitoring changes in morphological characteristics and examining cell viability, flow cytometry assays, and Western blot analyses.

Results: Combination of cordycepin plus cisplatin and/or paclitaxel for 12 and 24 hours induced apoptotic features in MA-10 cells. The MTT assay showed that the combination treatment reduced the viability of MA-10 cells in a dose-dependent manner, with additive effects. Cell cycle analysis showed that combination treatment significantly increased subG1 phase cell numbers in MA-10 cells, indicating apoptosis. Moreover, cordycepin plus cisplatin and/or paclitaxel significantly induced cleavage of caspase-8, caspase-9, caspase-3, and poly ADP-ribose polymerase, and phosphorylation of c-Jun NH2-terminal kinase, extracellular signal-regulated kinase, p38, and p53 proteins in MA-10 cells.

Conclusion: Cordycepin plus cisplatin and/or paclitaxel can have an additive effect on apoptosis in MA-10 cells, with activation of caspase, mitogen-activated protein kinase, and p53 signal pathways.

No MeSH data available.


Related in: MedlinePlus

Effects of cordycepin + paclitaxel and/or cisplatin on expression of phosphorylated JNK, ERK, and p38 protein in MA-10 cells.Notes: The cells were treated without or with 50 nM paclitaxel and/or 100 μM cisplatin +100 μM cordycepin for 12 and 24 hours. After treatment, the total JNK (54/46 kDa), phosphorylated JNK (54/46 kDa) (A), total ERK (42/44 kDa), phosphorylated ERK (42/44 kDa) (B), and total p38 (43 kDa) phosphorylated p38 (43 kDa) (C) proteins were detected by Western blot. The immunoblot represents the observations from one single experiment repeated at least three times. The integrated optical density of phosphorylated protein was analyzed after normalization with its total protein in each lane. Each datum point represents the mean ± standard error of the mean of three separate experiments. *Indicates that the means are significantly different compared with control (P<0.05).Abbreviations: Cor, cordycepin; Cis, cisplatin; DMSO, dimethyl sulfoxide; ERK, extracellular signal-regulated kinase; JNK, c-Jun NH2-terminal kinase; p-, phosphorylated; t-, total.
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f4-ott-8-2345: Effects of cordycepin + paclitaxel and/or cisplatin on expression of phosphorylated JNK, ERK, and p38 protein in MA-10 cells.Notes: The cells were treated without or with 50 nM paclitaxel and/or 100 μM cisplatin +100 μM cordycepin for 12 and 24 hours. After treatment, the total JNK (54/46 kDa), phosphorylated JNK (54/46 kDa) (A), total ERK (42/44 kDa), phosphorylated ERK (42/44 kDa) (B), and total p38 (43 kDa) phosphorylated p38 (43 kDa) (C) proteins were detected by Western blot. The immunoblot represents the observations from one single experiment repeated at least three times. The integrated optical density of phosphorylated protein was analyzed after normalization with its total protein in each lane. Each datum point represents the mean ± standard error of the mean of three separate experiments. *Indicates that the means are significantly different compared with control (P<0.05).Abbreviations: Cor, cordycepin; Cis, cisplatin; DMSO, dimethyl sulfoxide; ERK, extracellular signal-regulated kinase; JNK, c-Jun NH2-terminal kinase; p-, phosphorylated; t-, total.

Mentions: Previous studies have shown that activation of MAPK is involved in apoptosis induced by cordycepin, cisplatin, and paclitaxel in various tumor cells.30–32 Therefore, we investigated whether the MAPK pathway was involved in apoptosis stimulated by cordycepin + paclitaxel and/or cisplatin in MA-10 cells. Treatment with cordycepin for 12 and 24 hours, paclitaxel for 24 hours, cisplatin for 24 hours, cisplatin + cordycepin for 12 and 24 hours, cisplatin + paclitaxel for 24 hours, cordycepin + paclitaxel for 12 and 24 hours, and cordycepin + cisplatin + paclitaxel for 12 and 24 hours all significantly induce expression of phosphorylated JNK in MA-10 cells (P<0.05, Figure 4A). Only treatment with cordycepin, cisplatin + cordycepin, cordycepin + paclitaxel, and cordycepin + cisplatin + paclitaxel for 12 hours could induce significant expression of phosphorylated ERK in MA-10 cells (P<0.05, Figure 4B). Only treatment with cordycepin, cisplatin + cordycepin, cordycepin + paclitaxel, and cordycepin + cisplatin + paclitaxel for 24 hours could induce significant expression of phosphorylated p38 in MA-10 cells (P<0.05, Figure 4C). These results indicate that cordycepin + paclitaxel and/or cisplatin could stimulate phosphorylation of the JNK, ERK1/2, and p38 MAPK pathways to induce apoptosis in MA-10 cells.


Apoptotic effect of cordycepin combined with cisplatin and/or paclitaxel on MA-10 mouse Leydig tumor cells.

Kang FC, Chen PJ, Pan BS, Lai MS, Chen YC, Huang BM - Onco Targets Ther (2015)

Effects of cordycepin + paclitaxel and/or cisplatin on expression of phosphorylated JNK, ERK, and p38 protein in MA-10 cells.Notes: The cells were treated without or with 50 nM paclitaxel and/or 100 μM cisplatin +100 μM cordycepin for 12 and 24 hours. After treatment, the total JNK (54/46 kDa), phosphorylated JNK (54/46 kDa) (A), total ERK (42/44 kDa), phosphorylated ERK (42/44 kDa) (B), and total p38 (43 kDa) phosphorylated p38 (43 kDa) (C) proteins were detected by Western blot. The immunoblot represents the observations from one single experiment repeated at least three times. The integrated optical density of phosphorylated protein was analyzed after normalization with its total protein in each lane. Each datum point represents the mean ± standard error of the mean of three separate experiments. *Indicates that the means are significantly different compared with control (P<0.05).Abbreviations: Cor, cordycepin; Cis, cisplatin; DMSO, dimethyl sulfoxide; ERK, extracellular signal-regulated kinase; JNK, c-Jun NH2-terminal kinase; p-, phosphorylated; t-, total.
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f4-ott-8-2345: Effects of cordycepin + paclitaxel and/or cisplatin on expression of phosphorylated JNK, ERK, and p38 protein in MA-10 cells.Notes: The cells were treated without or with 50 nM paclitaxel and/or 100 μM cisplatin +100 μM cordycepin for 12 and 24 hours. After treatment, the total JNK (54/46 kDa), phosphorylated JNK (54/46 kDa) (A), total ERK (42/44 kDa), phosphorylated ERK (42/44 kDa) (B), and total p38 (43 kDa) phosphorylated p38 (43 kDa) (C) proteins were detected by Western blot. The immunoblot represents the observations from one single experiment repeated at least three times. The integrated optical density of phosphorylated protein was analyzed after normalization with its total protein in each lane. Each datum point represents the mean ± standard error of the mean of three separate experiments. *Indicates that the means are significantly different compared with control (P<0.05).Abbreviations: Cor, cordycepin; Cis, cisplatin; DMSO, dimethyl sulfoxide; ERK, extracellular signal-regulated kinase; JNK, c-Jun NH2-terminal kinase; p-, phosphorylated; t-, total.
Mentions: Previous studies have shown that activation of MAPK is involved in apoptosis induced by cordycepin, cisplatin, and paclitaxel in various tumor cells.30–32 Therefore, we investigated whether the MAPK pathway was involved in apoptosis stimulated by cordycepin + paclitaxel and/or cisplatin in MA-10 cells. Treatment with cordycepin for 12 and 24 hours, paclitaxel for 24 hours, cisplatin for 24 hours, cisplatin + cordycepin for 12 and 24 hours, cisplatin + paclitaxel for 24 hours, cordycepin + paclitaxel for 12 and 24 hours, and cordycepin + cisplatin + paclitaxel for 12 and 24 hours all significantly induce expression of phosphorylated JNK in MA-10 cells (P<0.05, Figure 4A). Only treatment with cordycepin, cisplatin + cordycepin, cordycepin + paclitaxel, and cordycepin + cisplatin + paclitaxel for 12 hours could induce significant expression of phosphorylated ERK in MA-10 cells (P<0.05, Figure 4B). Only treatment with cordycepin, cisplatin + cordycepin, cordycepin + paclitaxel, and cordycepin + cisplatin + paclitaxel for 24 hours could induce significant expression of phosphorylated p38 in MA-10 cells (P<0.05, Figure 4C). These results indicate that cordycepin + paclitaxel and/or cisplatin could stimulate phosphorylation of the JNK, ERK1/2, and p38 MAPK pathways to induce apoptosis in MA-10 cells.

Bottom Line: Cell cycle analysis showed that combination treatment significantly increased subG1 phase cell numbers in MA-10 cells, indicating apoptosis.Moreover, cordycepin plus cisplatin and/or paclitaxel significantly induced cleavage of caspase-8, caspase-9, caspase-3, and poly ADP-ribose polymerase, and phosphorylation of c-Jun NH2-terminal kinase, extracellular signal-regulated kinase, p38, and p53 proteins in MA-10 cells.Cordycepin plus cisplatin and/or paclitaxel can have an additive effect on apoptosis in MA-10 cells, with activation of caspase, mitogen-activated protein kinase, and p53 signal pathways.

View Article: PubMed Central - PubMed

Affiliation: Department of Anesthesia, Chi Mei Medical Center, Chiali, Republic of China.

ABSTRACT

Background: Chemotherapy is not limited to a single treatment, and the evidence demonstrates that different drug combinations can have positive results in patients. In this study, we sought to determine whether cordycepin combined with cisplatin and/or paclitaxel would have an additive effective on inducing apoptosis in mouse Leydig tumor cells, and the mechanisms were also briefly examined.

Methods: The additive effects of cordycepin combined with cisplatin and/or paclitaxel on apoptosis in MA-10 cells were investigated by monitoring changes in morphological characteristics and examining cell viability, flow cytometry assays, and Western blot analyses.

Results: Combination of cordycepin plus cisplatin and/or paclitaxel for 12 and 24 hours induced apoptotic features in MA-10 cells. The MTT assay showed that the combination treatment reduced the viability of MA-10 cells in a dose-dependent manner, with additive effects. Cell cycle analysis showed that combination treatment significantly increased subG1 phase cell numbers in MA-10 cells, indicating apoptosis. Moreover, cordycepin plus cisplatin and/or paclitaxel significantly induced cleavage of caspase-8, caspase-9, caspase-3, and poly ADP-ribose polymerase, and phosphorylation of c-Jun NH2-terminal kinase, extracellular signal-regulated kinase, p38, and p53 proteins in MA-10 cells.

Conclusion: Cordycepin plus cisplatin and/or paclitaxel can have an additive effect on apoptosis in MA-10 cells, with activation of caspase, mitogen-activated protein kinase, and p53 signal pathways.

No MeSH data available.


Related in: MedlinePlus