Midazolam induces apoptosis in MA-10 mouse leydig tumor cells through caspase activation and the involvement of MAPK signaling pathway

Edmund Cheung So, Yu Xuan Lin, Chi Hao Tseng, Bo Syong Pan, Ka Shun Cheng, Kar Lok Wong, Lyh Jyh Hao, Yang Kao Wang, Bu Miin Huang

研究成果: Article

6 引文 (Scopus)

摘要

Purpose: The present study aims to investigate how midazolam, a sedative drug for clinical use with cytotoxicity on neuronal and peripheral tissues, induced apoptosis in MA-10 mouse Leydig tumor cells. Methods: The apoptotic effect and underlying mechanism of midazolam to MA-10 cells were investigated by flow cytometry assay and Western blotting methods. Results: Data showed that midazolam induced the accumulation of the MA-10 cell population in the sub-G1 phase and a reduction in the G2/M phase in a time- and dose-dependent manner, suggesting an apoptotic phenomenon. Midazolam could also induce the activation of caspase-8, -9, and -3 and poly (ADP-ribose) polymerase proteins. There were no changes in the levels of Bax and cytochrome-c, whereas Bid was significantly decreased after midazolam treatment. Moreover, midazolam decreased both pAkt and Akt expression. In addition, midazolam stimulated the phosphorylation of p38 and c-Jun NH2-terminal kinase but not extracellular signal-regulated kinase. Conclusion: Midazolam could induce MA-10 cell apoptosis through the activation of caspase cascade, the inhibition of pAkt pathway, and the induction of p38 and c-Jun NH2-terminal kinase pathways.

原文English
頁(從 - 到)211-221
頁數11
期刊OncoTargets and Therapy
7
DOIs
出版狀態Published - 2014 二月 13

指紋

Leydig Cell Tumor
Midazolam
Caspases
Apoptosis
JNK Mitogen-Activated Protein Kinases
Poly(ADP-ribose) Polymerases
Caspase 9
Caspase 8
G2 Phase
Extracellular Signal-Regulated MAP Kinases
G1 Phase
Cytochromes c
Hypnotics and Sedatives
Cell Division
Flow Cytometry
Western Blotting
Phosphorylation

All Science Journal Classification (ASJC) codes

  • Oncology
  • Pharmacology (medical)

引用此文

So, Edmund Cheung ; Lin, Yu Xuan ; Tseng, Chi Hao ; Pan, Bo Syong ; Cheng, Ka Shun ; Wong, Kar Lok ; Hao, Lyh Jyh ; Wang, Yang Kao ; Huang, Bu Miin. / Midazolam induces apoptosis in MA-10 mouse leydig tumor cells through caspase activation and the involvement of MAPK signaling pathway. 於: OncoTargets and Therapy. 2014 ; 卷 7. 頁 211-221.
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abstract = "Purpose: The present study aims to investigate how midazolam, a sedative drug for clinical use with cytotoxicity on neuronal and peripheral tissues, induced apoptosis in MA-10 mouse Leydig tumor cells. Methods: The apoptotic effect and underlying mechanism of midazolam to MA-10 cells were investigated by flow cytometry assay and Western blotting methods. Results: Data showed that midazolam induced the accumulation of the MA-10 cell population in the sub-G1 phase and a reduction in the G2/M phase in a time- and dose-dependent manner, suggesting an apoptotic phenomenon. Midazolam could also induce the activation of caspase-8, -9, and -3 and poly (ADP-ribose) polymerase proteins. There were no changes in the levels of Bax and cytochrome-c, whereas Bid was significantly decreased after midazolam treatment. Moreover, midazolam decreased both pAkt and Akt expression. In addition, midazolam stimulated the phosphorylation of p38 and c-Jun NH2-terminal kinase but not extracellular signal-regulated kinase. Conclusion: Midazolam could induce MA-10 cell apoptosis through the activation of caspase cascade, the inhibition of pAkt pathway, and the induction of p38 and c-Jun NH2-terminal kinase pathways.",
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Midazolam induces apoptosis in MA-10 mouse leydig tumor cells through caspase activation and the involvement of MAPK signaling pathway. / So, Edmund Cheung; Lin, Yu Xuan; Tseng, Chi Hao; Pan, Bo Syong; Cheng, Ka Shun; Wong, Kar Lok; Hao, Lyh Jyh; Wang, Yang Kao; Huang, Bu Miin.

於: OncoTargets and Therapy, 卷 7, 13.02.2014, p. 211-221.

研究成果: Article

TY - JOUR

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AU - So, Edmund Cheung

AU - Lin, Yu Xuan

AU - Tseng, Chi Hao

AU - Pan, Bo Syong

AU - Cheng, Ka Shun

AU - Wong, Kar Lok

AU - Hao, Lyh Jyh

AU - Wang, Yang Kao

AU - Huang, Bu Miin

PY - 2014/2/13

Y1 - 2014/2/13

N2 - Purpose: The present study aims to investigate how midazolam, a sedative drug for clinical use with cytotoxicity on neuronal and peripheral tissues, induced apoptosis in MA-10 mouse Leydig tumor cells. Methods: The apoptotic effect and underlying mechanism of midazolam to MA-10 cells were investigated by flow cytometry assay and Western blotting methods. Results: Data showed that midazolam induced the accumulation of the MA-10 cell population in the sub-G1 phase and a reduction in the G2/M phase in a time- and dose-dependent manner, suggesting an apoptotic phenomenon. Midazolam could also induce the activation of caspase-8, -9, and -3 and poly (ADP-ribose) polymerase proteins. There were no changes in the levels of Bax and cytochrome-c, whereas Bid was significantly decreased after midazolam treatment. Moreover, midazolam decreased both pAkt and Akt expression. In addition, midazolam stimulated the phosphorylation of p38 and c-Jun NH2-terminal kinase but not extracellular signal-regulated kinase. Conclusion: Midazolam could induce MA-10 cell apoptosis through the activation of caspase cascade, the inhibition of pAkt pathway, and the induction of p38 and c-Jun NH2-terminal kinase pathways.

AB - Purpose: The present study aims to investigate how midazolam, a sedative drug for clinical use with cytotoxicity on neuronal and peripheral tissues, induced apoptosis in MA-10 mouse Leydig tumor cells. Methods: The apoptotic effect and underlying mechanism of midazolam to MA-10 cells were investigated by flow cytometry assay and Western blotting methods. Results: Data showed that midazolam induced the accumulation of the MA-10 cell population in the sub-G1 phase and a reduction in the G2/M phase in a time- and dose-dependent manner, suggesting an apoptotic phenomenon. Midazolam could also induce the activation of caspase-8, -9, and -3 and poly (ADP-ribose) polymerase proteins. There were no changes in the levels of Bax and cytochrome-c, whereas Bid was significantly decreased after midazolam treatment. Moreover, midazolam decreased both pAkt and Akt expression. In addition, midazolam stimulated the phosphorylation of p38 and c-Jun NH2-terminal kinase but not extracellular signal-regulated kinase. Conclusion: Midazolam could induce MA-10 cell apoptosis through the activation of caspase cascade, the inhibition of pAkt pathway, and the induction of p38 and c-Jun NH2-terminal kinase pathways.

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