Lobaplatin arrests cell cycle progression, induces apoptosis and impairs migration and invasion in B16-F10 melanoma cell line in vitro
Melanoma is highly resistant to most conventional treatment, and the incidence and mortality rates are increasing rapidly worldwide. The objective of this study was to determine the anticancer effects of lobaplatin on the melanoma carcinoma cell line B16-F10 in vitro, and explored its mechanisms of...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Yang, Fangfang [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2015transfer abstract |
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| Schlagwörter: |
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| Umfang: |
7 |
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| Übergeordnetes Werk: |
Enthalten in: A Scoping Review of Registered Clinical Trials of Cellular Therapy for COVID-19 and a - Liao, Gary ELSEVIER, 2020, Amsterdam [u.a.] |
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| Übergeordnetes Werk: |
volume:69 ; year:2015 ; pages:402-408 ; extent:7 |
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10.1016/j.biopha.2014.12.011 |
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| 245 | 1 | 0 | |a Lobaplatin arrests cell cycle progression, induces apoptosis and impairs migration and invasion in B16-F10 melanoma cell line in vitro |
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| 520 | |a Melanoma is highly resistant to most conventional treatment, and the incidence and mortality rates are increasing rapidly worldwide. The objective of this study was to determine the anticancer effects of lobaplatin on the melanoma carcinoma cell line B16-F10 in vitro, and explored its mechanisms of action. Our results have shown that lobaplatin inhibited cell proliferation in human melanoma A375 and CHL-1 cells and murine melanoma B16-F10 cells in a concentration- and time-dependent manner. Flow cytometry assay confirmed that lobaplatin affected B16-F10 cell survival by blocking cell cycle progression in G2/M phase and inducing apoptosis in a concentration-dependent manner. In addition, the apoptosis was associated with downregulation of anti-apoptotic protein Bcl-2 while upregulation of pro-apoptotic protein Bax. Lobaplatin could also decrease the mitochondrial membrane potential, indicating that lobaplatin may induce apoptosis via mitochondria-mediated apoptotic pathway. Furthermore, lobaplatin blocked B16-F10 cell migration and invasion in vitro. These results suggested that lobaplatin could be an effective chemotherapeutic agent in melanoma treatment by inhibiting proliferation, inducing apoptosis, cell cycle arrest and blocking cell migration and invasion. | ||
| 520 | |a Melanoma is highly resistant to most conventional treatment, and the incidence and mortality rates are increasing rapidly worldwide. The objective of this study was to determine the anticancer effects of lobaplatin on the melanoma carcinoma cell line B16-F10 in vitro, and explored its mechanisms of action. Our results have shown that lobaplatin inhibited cell proliferation in human melanoma A375 and CHL-1 cells and murine melanoma B16-F10 cells in a concentration- and time-dependent manner. Flow cytometry assay confirmed that lobaplatin affected B16-F10 cell survival by blocking cell cycle progression in G2/M phase and inducing apoptosis in a concentration-dependent manner. In addition, the apoptosis was associated with downregulation of anti-apoptotic protein Bcl-2 while upregulation of pro-apoptotic protein Bax. Lobaplatin could also decrease the mitochondrial membrane potential, indicating that lobaplatin may induce apoptosis via mitochondria-mediated apoptotic pathway. Furthermore, lobaplatin blocked B16-F10 cell migration and invasion in vitro. These results suggested that lobaplatin could be an effective chemotherapeutic agent in melanoma treatment by inhibiting proliferation, inducing apoptosis, cell cycle arrest and blocking cell migration and invasion. | ||
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| 700 | 1 | |a Wei, Yuquan |4 oth | |
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10.1016/j.biopha.2014.12.011 doi GBVA2015014000002.pica (DE-627)ELV029046912 (ELSEVIER)S0753-3322(14)00206-6 DE-627 ger DE-627 rakwb eng 610 610 DE-600 610 VZ 44.86 bkl Yang, Fangfang verfasserin aut Lobaplatin arrests cell cycle progression, induces apoptosis and impairs migration and invasion in B16-F10 melanoma cell line in vitro 2015transfer abstract 7 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Melanoma is highly resistant to most conventional treatment, and the incidence and mortality rates are increasing rapidly worldwide. The objective of this study was to determine the anticancer effects of lobaplatin on the melanoma carcinoma cell line B16-F10 in vitro, and explored its mechanisms of action. Our results have shown that lobaplatin inhibited cell proliferation in human melanoma A375 and CHL-1 cells and murine melanoma B16-F10 cells in a concentration- and time-dependent manner. Flow cytometry assay confirmed that lobaplatin affected B16-F10 cell survival by blocking cell cycle progression in G2/M phase and inducing apoptosis in a concentration-dependent manner. In addition, the apoptosis was associated with downregulation of anti-apoptotic protein Bcl-2 while upregulation of pro-apoptotic protein Bax. Lobaplatin could also decrease the mitochondrial membrane potential, indicating that lobaplatin may induce apoptosis via mitochondria-mediated apoptotic pathway. Furthermore, lobaplatin blocked B16-F10 cell migration and invasion in vitro. These results suggested that lobaplatin could be an effective chemotherapeutic agent in melanoma treatment by inhibiting proliferation, inducing apoptosis, cell cycle arrest and blocking cell migration and invasion. Melanoma is highly resistant to most conventional treatment, and the incidence and mortality rates are increasing rapidly worldwide. The objective of this study was to determine the anticancer effects of lobaplatin on the melanoma carcinoma cell line B16-F10 in vitro, and explored its mechanisms of action. Our results have shown that lobaplatin inhibited cell proliferation in human melanoma A375 and CHL-1 cells and murine melanoma B16-F10 cells in a concentration- and time-dependent manner. Flow cytometry assay confirmed that lobaplatin affected B16-F10 cell survival by blocking cell cycle progression in G2/M phase and inducing apoptosis in a concentration-dependent manner. In addition, the apoptosis was associated with downregulation of anti-apoptotic protein Bcl-2 while upregulation of pro-apoptotic protein Bax. Lobaplatin could also decrease the mitochondrial membrane potential, indicating that lobaplatin may induce apoptosis via mitochondria-mediated apoptotic pathway. Furthermore, lobaplatin blocked B16-F10 cell migration and invasion in vitro. These results suggested that lobaplatin could be an effective chemotherapeutic agent in melanoma treatment by inhibiting proliferation, inducing apoptosis, cell cycle arrest and blocking cell migration and invasion. PBS Elsevier FCM Elsevier SDS-PAGE Elsevier SD Elsevier DMSO Elsevier FBS Elsevier PI Elsevier ΔΨ m Elsevier MTT Elsevier PVDF Elsevier Rh123 Elsevier Yu, Yang oth Lei, Qian oth Zeng, Anqi oth Li, Yali oth Xie, Yongmei oth Ye, TingHong oth Wei, Yuquan oth Enthalten in Elsevier Science Liao, Gary ELSEVIER A Scoping Review of Registered Clinical Trials of Cellular Therapy for COVID-19 and a 2020 Amsterdam [u.a.] (DE-627)ELV004620771 volume:69 year:2015 pages:402-408 extent:7 https://doi.org/10.1016/j.biopha.2014.12.011 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 44.86 Hämatologie VZ AR 69 2015 402-408 7 045F 610 |
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10.1016/j.biopha.2014.12.011 doi GBVA2015014000002.pica (DE-627)ELV029046912 (ELSEVIER)S0753-3322(14)00206-6 DE-627 ger DE-627 rakwb eng 610 610 DE-600 610 VZ 44.86 bkl Yang, Fangfang verfasserin aut Lobaplatin arrests cell cycle progression, induces apoptosis and impairs migration and invasion in B16-F10 melanoma cell line in vitro 2015transfer abstract 7 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Melanoma is highly resistant to most conventional treatment, and the incidence and mortality rates are increasing rapidly worldwide. The objective of this study was to determine the anticancer effects of lobaplatin on the melanoma carcinoma cell line B16-F10 in vitro, and explored its mechanisms of action. Our results have shown that lobaplatin inhibited cell proliferation in human melanoma A375 and CHL-1 cells and murine melanoma B16-F10 cells in a concentration- and time-dependent manner. Flow cytometry assay confirmed that lobaplatin affected B16-F10 cell survival by blocking cell cycle progression in G2/M phase and inducing apoptosis in a concentration-dependent manner. In addition, the apoptosis was associated with downregulation of anti-apoptotic protein Bcl-2 while upregulation of pro-apoptotic protein Bax. Lobaplatin could also decrease the mitochondrial membrane potential, indicating that lobaplatin may induce apoptosis via mitochondria-mediated apoptotic pathway. Furthermore, lobaplatin blocked B16-F10 cell migration and invasion in vitro. These results suggested that lobaplatin could be an effective chemotherapeutic agent in melanoma treatment by inhibiting proliferation, inducing apoptosis, cell cycle arrest and blocking cell migration and invasion. Melanoma is highly resistant to most conventional treatment, and the incidence and mortality rates are increasing rapidly worldwide. The objective of this study was to determine the anticancer effects of lobaplatin on the melanoma carcinoma cell line B16-F10 in vitro, and explored its mechanisms of action. Our results have shown that lobaplatin inhibited cell proliferation in human melanoma A375 and CHL-1 cells and murine melanoma B16-F10 cells in a concentration- and time-dependent manner. Flow cytometry assay confirmed that lobaplatin affected B16-F10 cell survival by blocking cell cycle progression in G2/M phase and inducing apoptosis in a concentration-dependent manner. In addition, the apoptosis was associated with downregulation of anti-apoptotic protein Bcl-2 while upregulation of pro-apoptotic protein Bax. Lobaplatin could also decrease the mitochondrial membrane potential, indicating that lobaplatin may induce apoptosis via mitochondria-mediated apoptotic pathway. Furthermore, lobaplatin blocked B16-F10 cell migration and invasion in vitro. These results suggested that lobaplatin could be an effective chemotherapeutic agent in melanoma treatment by inhibiting proliferation, inducing apoptosis, cell cycle arrest and blocking cell migration and invasion. PBS Elsevier FCM Elsevier SDS-PAGE Elsevier SD Elsevier DMSO Elsevier FBS Elsevier PI Elsevier ΔΨ m Elsevier MTT Elsevier PVDF Elsevier Rh123 Elsevier Yu, Yang oth Lei, Qian oth Zeng, Anqi oth Li, Yali oth Xie, Yongmei oth Ye, TingHong oth Wei, Yuquan oth Enthalten in Elsevier Science Liao, Gary ELSEVIER A Scoping Review of Registered Clinical Trials of Cellular Therapy for COVID-19 and a 2020 Amsterdam [u.a.] (DE-627)ELV004620771 volume:69 year:2015 pages:402-408 extent:7 https://doi.org/10.1016/j.biopha.2014.12.011 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 44.86 Hämatologie VZ AR 69 2015 402-408 7 045F 610 |
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10.1016/j.biopha.2014.12.011 doi GBVA2015014000002.pica (DE-627)ELV029046912 (ELSEVIER)S0753-3322(14)00206-6 DE-627 ger DE-627 rakwb eng 610 610 DE-600 610 VZ 44.86 bkl Yang, Fangfang verfasserin aut Lobaplatin arrests cell cycle progression, induces apoptosis and impairs migration and invasion in B16-F10 melanoma cell line in vitro 2015transfer abstract 7 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Melanoma is highly resistant to most conventional treatment, and the incidence and mortality rates are increasing rapidly worldwide. The objective of this study was to determine the anticancer effects of lobaplatin on the melanoma carcinoma cell line B16-F10 in vitro, and explored its mechanisms of action. Our results have shown that lobaplatin inhibited cell proliferation in human melanoma A375 and CHL-1 cells and murine melanoma B16-F10 cells in a concentration- and time-dependent manner. Flow cytometry assay confirmed that lobaplatin affected B16-F10 cell survival by blocking cell cycle progression in G2/M phase and inducing apoptosis in a concentration-dependent manner. In addition, the apoptosis was associated with downregulation of anti-apoptotic protein Bcl-2 while upregulation of pro-apoptotic protein Bax. Lobaplatin could also decrease the mitochondrial membrane potential, indicating that lobaplatin may induce apoptosis via mitochondria-mediated apoptotic pathway. Furthermore, lobaplatin blocked B16-F10 cell migration and invasion in vitro. These results suggested that lobaplatin could be an effective chemotherapeutic agent in melanoma treatment by inhibiting proliferation, inducing apoptosis, cell cycle arrest and blocking cell migration and invasion. Melanoma is highly resistant to most conventional treatment, and the incidence and mortality rates are increasing rapidly worldwide. The objective of this study was to determine the anticancer effects of lobaplatin on the melanoma carcinoma cell line B16-F10 in vitro, and explored its mechanisms of action. Our results have shown that lobaplatin inhibited cell proliferation in human melanoma A375 and CHL-1 cells and murine melanoma B16-F10 cells in a concentration- and time-dependent manner. Flow cytometry assay confirmed that lobaplatin affected B16-F10 cell survival by blocking cell cycle progression in G2/M phase and inducing apoptosis in a concentration-dependent manner. In addition, the apoptosis was associated with downregulation of anti-apoptotic protein Bcl-2 while upregulation of pro-apoptotic protein Bax. Lobaplatin could also decrease the mitochondrial membrane potential, indicating that lobaplatin may induce apoptosis via mitochondria-mediated apoptotic pathway. Furthermore, lobaplatin blocked B16-F10 cell migration and invasion in vitro. These results suggested that lobaplatin could be an effective chemotherapeutic agent in melanoma treatment by inhibiting proliferation, inducing apoptosis, cell cycle arrest and blocking cell migration and invasion. PBS Elsevier FCM Elsevier SDS-PAGE Elsevier SD Elsevier DMSO Elsevier FBS Elsevier PI Elsevier ΔΨ m Elsevier MTT Elsevier PVDF Elsevier Rh123 Elsevier Yu, Yang oth Lei, Qian oth Zeng, Anqi oth Li, Yali oth Xie, Yongmei oth Ye, TingHong oth Wei, Yuquan oth Enthalten in Elsevier Science Liao, Gary ELSEVIER A Scoping Review of Registered Clinical Trials of Cellular Therapy for COVID-19 and a 2020 Amsterdam [u.a.] (DE-627)ELV004620771 volume:69 year:2015 pages:402-408 extent:7 https://doi.org/10.1016/j.biopha.2014.12.011 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 44.86 Hämatologie VZ AR 69 2015 402-408 7 045F 610 |
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10.1016/j.biopha.2014.12.011 doi GBVA2015014000002.pica (DE-627)ELV029046912 (ELSEVIER)S0753-3322(14)00206-6 DE-627 ger DE-627 rakwb eng 610 610 DE-600 610 VZ 44.86 bkl Yang, Fangfang verfasserin aut Lobaplatin arrests cell cycle progression, induces apoptosis and impairs migration and invasion in B16-F10 melanoma cell line in vitro 2015transfer abstract 7 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Melanoma is highly resistant to most conventional treatment, and the incidence and mortality rates are increasing rapidly worldwide. The objective of this study was to determine the anticancer effects of lobaplatin on the melanoma carcinoma cell line B16-F10 in vitro, and explored its mechanisms of action. Our results have shown that lobaplatin inhibited cell proliferation in human melanoma A375 and CHL-1 cells and murine melanoma B16-F10 cells in a concentration- and time-dependent manner. Flow cytometry assay confirmed that lobaplatin affected B16-F10 cell survival by blocking cell cycle progression in G2/M phase and inducing apoptosis in a concentration-dependent manner. In addition, the apoptosis was associated with downregulation of anti-apoptotic protein Bcl-2 while upregulation of pro-apoptotic protein Bax. Lobaplatin could also decrease the mitochondrial membrane potential, indicating that lobaplatin may induce apoptosis via mitochondria-mediated apoptotic pathway. Furthermore, lobaplatin blocked B16-F10 cell migration and invasion in vitro. These results suggested that lobaplatin could be an effective chemotherapeutic agent in melanoma treatment by inhibiting proliferation, inducing apoptosis, cell cycle arrest and blocking cell migration and invasion. Melanoma is highly resistant to most conventional treatment, and the incidence and mortality rates are increasing rapidly worldwide. The objective of this study was to determine the anticancer effects of lobaplatin on the melanoma carcinoma cell line B16-F10 in vitro, and explored its mechanisms of action. Our results have shown that lobaplatin inhibited cell proliferation in human melanoma A375 and CHL-1 cells and murine melanoma B16-F10 cells in a concentration- and time-dependent manner. Flow cytometry assay confirmed that lobaplatin affected B16-F10 cell survival by blocking cell cycle progression in G2/M phase and inducing apoptosis in a concentration-dependent manner. In addition, the apoptosis was associated with downregulation of anti-apoptotic protein Bcl-2 while upregulation of pro-apoptotic protein Bax. Lobaplatin could also decrease the mitochondrial membrane potential, indicating that lobaplatin may induce apoptosis via mitochondria-mediated apoptotic pathway. Furthermore, lobaplatin blocked B16-F10 cell migration and invasion in vitro. These results suggested that lobaplatin could be an effective chemotherapeutic agent in melanoma treatment by inhibiting proliferation, inducing apoptosis, cell cycle arrest and blocking cell migration and invasion. PBS Elsevier FCM Elsevier SDS-PAGE Elsevier SD Elsevier DMSO Elsevier FBS Elsevier PI Elsevier ΔΨ m Elsevier MTT Elsevier PVDF Elsevier Rh123 Elsevier Yu, Yang oth Lei, Qian oth Zeng, Anqi oth Li, Yali oth Xie, Yongmei oth Ye, TingHong oth Wei, Yuquan oth Enthalten in Elsevier Science Liao, Gary ELSEVIER A Scoping Review of Registered Clinical Trials of Cellular Therapy for COVID-19 and a 2020 Amsterdam [u.a.] (DE-627)ELV004620771 volume:69 year:2015 pages:402-408 extent:7 https://doi.org/10.1016/j.biopha.2014.12.011 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 44.86 Hämatologie VZ AR 69 2015 402-408 7 045F 610 |
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10.1016/j.biopha.2014.12.011 doi GBVA2015014000002.pica (DE-627)ELV029046912 (ELSEVIER)S0753-3322(14)00206-6 DE-627 ger DE-627 rakwb eng 610 610 DE-600 610 VZ 44.86 bkl Yang, Fangfang verfasserin aut Lobaplatin arrests cell cycle progression, induces apoptosis and impairs migration and invasion in B16-F10 melanoma cell line in vitro 2015transfer abstract 7 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Melanoma is highly resistant to most conventional treatment, and the incidence and mortality rates are increasing rapidly worldwide. The objective of this study was to determine the anticancer effects of lobaplatin on the melanoma carcinoma cell line B16-F10 in vitro, and explored its mechanisms of action. Our results have shown that lobaplatin inhibited cell proliferation in human melanoma A375 and CHL-1 cells and murine melanoma B16-F10 cells in a concentration- and time-dependent manner. Flow cytometry assay confirmed that lobaplatin affected B16-F10 cell survival by blocking cell cycle progression in G2/M phase and inducing apoptosis in a concentration-dependent manner. In addition, the apoptosis was associated with downregulation of anti-apoptotic protein Bcl-2 while upregulation of pro-apoptotic protein Bax. Lobaplatin could also decrease the mitochondrial membrane potential, indicating that lobaplatin may induce apoptosis via mitochondria-mediated apoptotic pathway. Furthermore, lobaplatin blocked B16-F10 cell migration and invasion in vitro. These results suggested that lobaplatin could be an effective chemotherapeutic agent in melanoma treatment by inhibiting proliferation, inducing apoptosis, cell cycle arrest and blocking cell migration and invasion. Melanoma is highly resistant to most conventional treatment, and the incidence and mortality rates are increasing rapidly worldwide. The objective of this study was to determine the anticancer effects of lobaplatin on the melanoma carcinoma cell line B16-F10 in vitro, and explored its mechanisms of action. Our results have shown that lobaplatin inhibited cell proliferation in human melanoma A375 and CHL-1 cells and murine melanoma B16-F10 cells in a concentration- and time-dependent manner. Flow cytometry assay confirmed that lobaplatin affected B16-F10 cell survival by blocking cell cycle progression in G2/M phase and inducing apoptosis in a concentration-dependent manner. In addition, the apoptosis was associated with downregulation of anti-apoptotic protein Bcl-2 while upregulation of pro-apoptotic protein Bax. Lobaplatin could also decrease the mitochondrial membrane potential, indicating that lobaplatin may induce apoptosis via mitochondria-mediated apoptotic pathway. Furthermore, lobaplatin blocked B16-F10 cell migration and invasion in vitro. These results suggested that lobaplatin could be an effective chemotherapeutic agent in melanoma treatment by inhibiting proliferation, inducing apoptosis, cell cycle arrest and blocking cell migration and invasion. PBS Elsevier FCM Elsevier SDS-PAGE Elsevier SD Elsevier DMSO Elsevier FBS Elsevier PI Elsevier ΔΨ m Elsevier MTT Elsevier PVDF Elsevier Rh123 Elsevier Yu, Yang oth Lei, Qian oth Zeng, Anqi oth Li, Yali oth Xie, Yongmei oth Ye, TingHong oth Wei, Yuquan oth Enthalten in Elsevier Science Liao, Gary ELSEVIER A Scoping Review of Registered Clinical Trials of Cellular Therapy for COVID-19 and a 2020 Amsterdam [u.a.] (DE-627)ELV004620771 volume:69 year:2015 pages:402-408 extent:7 https://doi.org/10.1016/j.biopha.2014.12.011 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 44.86 Hämatologie VZ AR 69 2015 402-408 7 045F 610 |
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lobaplatin arrests cell cycle progression, induces apoptosis and impairs migration and invasion in b16-f10 melanoma cell line in vitro |
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Lobaplatin arrests cell cycle progression, induces apoptosis and impairs migration and invasion in B16-F10 melanoma cell line in vitro |
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Melanoma is highly resistant to most conventional treatment, and the incidence and mortality rates are increasing rapidly worldwide. The objective of this study was to determine the anticancer effects of lobaplatin on the melanoma carcinoma cell line B16-F10 in vitro, and explored its mechanisms of action. Our results have shown that lobaplatin inhibited cell proliferation in human melanoma A375 and CHL-1 cells and murine melanoma B16-F10 cells in a concentration- and time-dependent manner. Flow cytometry assay confirmed that lobaplatin affected B16-F10 cell survival by blocking cell cycle progression in G2/M phase and inducing apoptosis in a concentration-dependent manner. In addition, the apoptosis was associated with downregulation of anti-apoptotic protein Bcl-2 while upregulation of pro-apoptotic protein Bax. Lobaplatin could also decrease the mitochondrial membrane potential, indicating that lobaplatin may induce apoptosis via mitochondria-mediated apoptotic pathway. Furthermore, lobaplatin blocked B16-F10 cell migration and invasion in vitro. These results suggested that lobaplatin could be an effective chemotherapeutic agent in melanoma treatment by inhibiting proliferation, inducing apoptosis, cell cycle arrest and blocking cell migration and invasion. |
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Melanoma is highly resistant to most conventional treatment, and the incidence and mortality rates are increasing rapidly worldwide. The objective of this study was to determine the anticancer effects of lobaplatin on the melanoma carcinoma cell line B16-F10 in vitro, and explored its mechanisms of action. Our results have shown that lobaplatin inhibited cell proliferation in human melanoma A375 and CHL-1 cells and murine melanoma B16-F10 cells in a concentration- and time-dependent manner. Flow cytometry assay confirmed that lobaplatin affected B16-F10 cell survival by blocking cell cycle progression in G2/M phase and inducing apoptosis in a concentration-dependent manner. In addition, the apoptosis was associated with downregulation of anti-apoptotic protein Bcl-2 while upregulation of pro-apoptotic protein Bax. Lobaplatin could also decrease the mitochondrial membrane potential, indicating that lobaplatin may induce apoptosis via mitochondria-mediated apoptotic pathway. Furthermore, lobaplatin blocked B16-F10 cell migration and invasion in vitro. These results suggested that lobaplatin could be an effective chemotherapeutic agent in melanoma treatment by inhibiting proliferation, inducing apoptosis, cell cycle arrest and blocking cell migration and invasion. |
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Melanoma is highly resistant to most conventional treatment, and the incidence and mortality rates are increasing rapidly worldwide. The objective of this study was to determine the anticancer effects of lobaplatin on the melanoma carcinoma cell line B16-F10 in vitro, and explored its mechanisms of action. Our results have shown that lobaplatin inhibited cell proliferation in human melanoma A375 and CHL-1 cells and murine melanoma B16-F10 cells in a concentration- and time-dependent manner. Flow cytometry assay confirmed that lobaplatin affected B16-F10 cell survival by blocking cell cycle progression in G2/M phase and inducing apoptosis in a concentration-dependent manner. In addition, the apoptosis was associated with downregulation of anti-apoptotic protein Bcl-2 while upregulation of pro-apoptotic protein Bax. Lobaplatin could also decrease the mitochondrial membrane potential, indicating that lobaplatin may induce apoptosis via mitochondria-mediated apoptotic pathway. Furthermore, lobaplatin blocked B16-F10 cell migration and invasion in vitro. These results suggested that lobaplatin could be an effective chemotherapeutic agent in melanoma treatment by inhibiting proliferation, inducing apoptosis, cell cycle arrest and blocking cell migration and invasion. |
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