Valproic acid overcomes sorafenib resistance by reducing the migration of Jagged2-mediated Notch1 signaling pathway in hepatocellular carcinoma cells
Sorafenib resistance is a classic problem related to the treatment of advanced hepatocellular carcinoma (HCC). There is a recognized need to explore new drug resistance mechanisms and develop novel strategies to overcome the acquired resistance to sorafenib. Although one study has showed that the an...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Liu, Jing [verfasserIn] |
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| Format: |
E-Artikel |
|---|---|
| Sprache: |
Englisch |
| Erschienen: |
2020transfer abstract |
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| Schlagwörter: |
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| Übergeordnetes Werk: |
Enthalten in: Urological Diseases of the Byzantine Emperors (330-1453) - 2011, Amsterdam |
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| Übergeordnetes Werk: |
volume:126 ; year:2020 ; pages:0 |
| Links: |
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| DOI / URN: |
10.1016/j.biocel.2020.105820 |
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| 245 | 1 | 0 | |a Valproic acid overcomes sorafenib resistance by reducing the migration of Jagged2-mediated Notch1 signaling pathway in hepatocellular carcinoma cells |
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| 520 | |a Sorafenib resistance is a classic problem related to the treatment of advanced hepatocellular carcinoma (HCC). There is a recognized need to explore new drug resistance mechanisms and develop novel strategies to overcome the acquired resistance to sorafenib. Although one study has showed that the anti-epileptic drug valproic acid (VPA) could sensitize transforming growth factor-β (TGF-β)-induced sorafenib-resistant HCC cells, it is unclear whether VPA could reverse resistance to long-term clinical treatment with sorafenib. In this study, we successfully established sorafenib-resistant HCC cells by long-term sorafenib exposure. Compared with sensitive HCC cells, the proliferation, anti-apoptotic capability and migration of the sorafenib-resistant cells were enhanced. In addition, we found that VPA combined with sorafenib could overcome drug resistance by downregulating Jagged2-mediated Notch1 signaling pathway and epithelial-mesenchymal transition (EMT)-related proteins. Furthermore, the combination of VPA and sorafenib could obviously increase the sensitivity of drug-resistant cells in vitro and synergistically suppress tumor growth in vivo. These results provided a new insight that the use of VPA in combination with sorafenib was an effective method for clinically solving the problem of sorafenib resistance by modulating the Jagged2-mediated Notch1 signaling pathway and reversing the EMT phenotype. | ||
| 520 | |a Sorafenib resistance is a classic problem related to the treatment of advanced hepatocellular carcinoma (HCC). There is a recognized need to explore new drug resistance mechanisms and develop novel strategies to overcome the acquired resistance to sorafenib. Although one study has showed that the anti-epileptic drug valproic acid (VPA) could sensitize transforming growth factor-β (TGF-β)-induced sorafenib-resistant HCC cells, it is unclear whether VPA could reverse resistance to long-term clinical treatment with sorafenib. In this study, we successfully established sorafenib-resistant HCC cells by long-term sorafenib exposure. Compared with sensitive HCC cells, the proliferation, anti-apoptotic capability and migration of the sorafenib-resistant cells were enhanced. In addition, we found that VPA combined with sorafenib could overcome drug resistance by downregulating Jagged2-mediated Notch1 signaling pathway and epithelial-mesenchymal transition (EMT)-related proteins. Furthermore, the combination of VPA and sorafenib could obviously increase the sensitivity of drug-resistant cells in vitro and synergistically suppress tumor growth in vivo. These results provided a new insight that the use of VPA in combination with sorafenib was an effective method for clinically solving the problem of sorafenib resistance by modulating the Jagged2-mediated Notch1 signaling pathway and reversing the EMT phenotype. | ||
| 650 | 7 | |a Jagged2 |2 Elsevier | |
| 650 | 7 | |a Notch1 |2 Elsevier | |
| 650 | 7 | |a Migration |2 Elsevier | |
| 650 | 7 | |a Sorafenib resistance |2 Elsevier | |
| 650 | 7 | |a Valproic acid |2 Elsevier | |
| 700 | 1 | |a Yang, Xu |4 oth | |
| 700 | 1 | |a Liang, Qing |4 oth | |
| 700 | 1 | |a Yu, Yan |4 oth | |
| 700 | 1 | |a Shen, Xiaoying |4 oth | |
| 700 | 1 | |a Sun, Guangchun |4 oth | |
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10.1016/j.biocel.2020.105820 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001117.pica (DE-627)ELV051206706 (ELSEVIER)S1357-2725(20)30137-0 DE-627 ger DE-627 rakwb eng 610 VZ 610 VZ 44.85 bkl Liu, Jing verfasserin aut Valproic acid overcomes sorafenib resistance by reducing the migration of Jagged2-mediated Notch1 signaling pathway in hepatocellular carcinoma cells 2020transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Sorafenib resistance is a classic problem related to the treatment of advanced hepatocellular carcinoma (HCC). There is a recognized need to explore new drug resistance mechanisms and develop novel strategies to overcome the acquired resistance to sorafenib. Although one study has showed that the anti-epileptic drug valproic acid (VPA) could sensitize transforming growth factor-β (TGF-β)-induced sorafenib-resistant HCC cells, it is unclear whether VPA could reverse resistance to long-term clinical treatment with sorafenib. In this study, we successfully established sorafenib-resistant HCC cells by long-term sorafenib exposure. Compared with sensitive HCC cells, the proliferation, anti-apoptotic capability and migration of the sorafenib-resistant cells were enhanced. In addition, we found that VPA combined with sorafenib could overcome drug resistance by downregulating Jagged2-mediated Notch1 signaling pathway and epithelial-mesenchymal transition (EMT)-related proteins. Furthermore, the combination of VPA and sorafenib could obviously increase the sensitivity of drug-resistant cells in vitro and synergistically suppress tumor growth in vivo. These results provided a new insight that the use of VPA in combination with sorafenib was an effective method for clinically solving the problem of sorafenib resistance by modulating the Jagged2-mediated Notch1 signaling pathway and reversing the EMT phenotype. Sorafenib resistance is a classic problem related to the treatment of advanced hepatocellular carcinoma (HCC). There is a recognized need to explore new drug resistance mechanisms and develop novel strategies to overcome the acquired resistance to sorafenib. Although one study has showed that the anti-epileptic drug valproic acid (VPA) could sensitize transforming growth factor-β (TGF-β)-induced sorafenib-resistant HCC cells, it is unclear whether VPA could reverse resistance to long-term clinical treatment with sorafenib. In this study, we successfully established sorafenib-resistant HCC cells by long-term sorafenib exposure. Compared with sensitive HCC cells, the proliferation, anti-apoptotic capability and migration of the sorafenib-resistant cells were enhanced. In addition, we found that VPA combined with sorafenib could overcome drug resistance by downregulating Jagged2-mediated Notch1 signaling pathway and epithelial-mesenchymal transition (EMT)-related proteins. Furthermore, the combination of VPA and sorafenib could obviously increase the sensitivity of drug-resistant cells in vitro and synergistically suppress tumor growth in vivo. These results provided a new insight that the use of VPA in combination with sorafenib was an effective method for clinically solving the problem of sorafenib resistance by modulating the Jagged2-mediated Notch1 signaling pathway and reversing the EMT phenotype. Jagged2 Elsevier Notch1 Elsevier Migration Elsevier Sorafenib resistance Elsevier Valproic acid Elsevier Yang, Xu oth Liang, Qing oth Yu, Yan oth Shen, Xiaoying oth Sun, Guangchun oth Enthalten in Elsevier Urological Diseases of the Byzantine Emperors (330-1453) 2011 Amsterdam (DE-627)ELV010616845 volume:126 year:2020 pages:0 https://doi.org/10.1016/j.biocel.2020.105820 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 44.85 Kardiologie Angiologie VZ AR 126 2020 0 |
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10.1016/j.biocel.2020.105820 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001117.pica (DE-627)ELV051206706 (ELSEVIER)S1357-2725(20)30137-0 DE-627 ger DE-627 rakwb eng 610 VZ 610 VZ 44.85 bkl Liu, Jing verfasserin aut Valproic acid overcomes sorafenib resistance by reducing the migration of Jagged2-mediated Notch1 signaling pathway in hepatocellular carcinoma cells 2020transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Sorafenib resistance is a classic problem related to the treatment of advanced hepatocellular carcinoma (HCC). There is a recognized need to explore new drug resistance mechanisms and develop novel strategies to overcome the acquired resistance to sorafenib. Although one study has showed that the anti-epileptic drug valproic acid (VPA) could sensitize transforming growth factor-β (TGF-β)-induced sorafenib-resistant HCC cells, it is unclear whether VPA could reverse resistance to long-term clinical treatment with sorafenib. In this study, we successfully established sorafenib-resistant HCC cells by long-term sorafenib exposure. Compared with sensitive HCC cells, the proliferation, anti-apoptotic capability and migration of the sorafenib-resistant cells were enhanced. In addition, we found that VPA combined with sorafenib could overcome drug resistance by downregulating Jagged2-mediated Notch1 signaling pathway and epithelial-mesenchymal transition (EMT)-related proteins. Furthermore, the combination of VPA and sorafenib could obviously increase the sensitivity of drug-resistant cells in vitro and synergistically suppress tumor growth in vivo. These results provided a new insight that the use of VPA in combination with sorafenib was an effective method for clinically solving the problem of sorafenib resistance by modulating the Jagged2-mediated Notch1 signaling pathway and reversing the EMT phenotype. Sorafenib resistance is a classic problem related to the treatment of advanced hepatocellular carcinoma (HCC). There is a recognized need to explore new drug resistance mechanisms and develop novel strategies to overcome the acquired resistance to sorafenib. Although one study has showed that the anti-epileptic drug valproic acid (VPA) could sensitize transforming growth factor-β (TGF-β)-induced sorafenib-resistant HCC cells, it is unclear whether VPA could reverse resistance to long-term clinical treatment with sorafenib. In this study, we successfully established sorafenib-resistant HCC cells by long-term sorafenib exposure. Compared with sensitive HCC cells, the proliferation, anti-apoptotic capability and migration of the sorafenib-resistant cells were enhanced. In addition, we found that VPA combined with sorafenib could overcome drug resistance by downregulating Jagged2-mediated Notch1 signaling pathway and epithelial-mesenchymal transition (EMT)-related proteins. Furthermore, the combination of VPA and sorafenib could obviously increase the sensitivity of drug-resistant cells in vitro and synergistically suppress tumor growth in vivo. These results provided a new insight that the use of VPA in combination with sorafenib was an effective method for clinically solving the problem of sorafenib resistance by modulating the Jagged2-mediated Notch1 signaling pathway and reversing the EMT phenotype. Jagged2 Elsevier Notch1 Elsevier Migration Elsevier Sorafenib resistance Elsevier Valproic acid Elsevier Yang, Xu oth Liang, Qing oth Yu, Yan oth Shen, Xiaoying oth Sun, Guangchun oth Enthalten in Elsevier Urological Diseases of the Byzantine Emperors (330-1453) 2011 Amsterdam (DE-627)ELV010616845 volume:126 year:2020 pages:0 https://doi.org/10.1016/j.biocel.2020.105820 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 44.85 Kardiologie Angiologie VZ AR 126 2020 0 |
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10.1016/j.biocel.2020.105820 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001117.pica (DE-627)ELV051206706 (ELSEVIER)S1357-2725(20)30137-0 DE-627 ger DE-627 rakwb eng 610 VZ 610 VZ 44.85 bkl Liu, Jing verfasserin aut Valproic acid overcomes sorafenib resistance by reducing the migration of Jagged2-mediated Notch1 signaling pathway in hepatocellular carcinoma cells 2020transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Sorafenib resistance is a classic problem related to the treatment of advanced hepatocellular carcinoma (HCC). There is a recognized need to explore new drug resistance mechanisms and develop novel strategies to overcome the acquired resistance to sorafenib. Although one study has showed that the anti-epileptic drug valproic acid (VPA) could sensitize transforming growth factor-β (TGF-β)-induced sorafenib-resistant HCC cells, it is unclear whether VPA could reverse resistance to long-term clinical treatment with sorafenib. In this study, we successfully established sorafenib-resistant HCC cells by long-term sorafenib exposure. Compared with sensitive HCC cells, the proliferation, anti-apoptotic capability and migration of the sorafenib-resistant cells were enhanced. In addition, we found that VPA combined with sorafenib could overcome drug resistance by downregulating Jagged2-mediated Notch1 signaling pathway and epithelial-mesenchymal transition (EMT)-related proteins. Furthermore, the combination of VPA and sorafenib could obviously increase the sensitivity of drug-resistant cells in vitro and synergistically suppress tumor growth in vivo. These results provided a new insight that the use of VPA in combination with sorafenib was an effective method for clinically solving the problem of sorafenib resistance by modulating the Jagged2-mediated Notch1 signaling pathway and reversing the EMT phenotype. Sorafenib resistance is a classic problem related to the treatment of advanced hepatocellular carcinoma (HCC). There is a recognized need to explore new drug resistance mechanisms and develop novel strategies to overcome the acquired resistance to sorafenib. Although one study has showed that the anti-epileptic drug valproic acid (VPA) could sensitize transforming growth factor-β (TGF-β)-induced sorafenib-resistant HCC cells, it is unclear whether VPA could reverse resistance to long-term clinical treatment with sorafenib. In this study, we successfully established sorafenib-resistant HCC cells by long-term sorafenib exposure. Compared with sensitive HCC cells, the proliferation, anti-apoptotic capability and migration of the sorafenib-resistant cells were enhanced. In addition, we found that VPA combined with sorafenib could overcome drug resistance by downregulating Jagged2-mediated Notch1 signaling pathway and epithelial-mesenchymal transition (EMT)-related proteins. Furthermore, the combination of VPA and sorafenib could obviously increase the sensitivity of drug-resistant cells in vitro and synergistically suppress tumor growth in vivo. These results provided a new insight that the use of VPA in combination with sorafenib was an effective method for clinically solving the problem of sorafenib resistance by modulating the Jagged2-mediated Notch1 signaling pathway and reversing the EMT phenotype. Jagged2 Elsevier Notch1 Elsevier Migration Elsevier Sorafenib resistance Elsevier Valproic acid Elsevier Yang, Xu oth Liang, Qing oth Yu, Yan oth Shen, Xiaoying oth Sun, Guangchun oth Enthalten in Elsevier Urological Diseases of the Byzantine Emperors (330-1453) 2011 Amsterdam (DE-627)ELV010616845 volume:126 year:2020 pages:0 https://doi.org/10.1016/j.biocel.2020.105820 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 44.85 Kardiologie Angiologie VZ AR 126 2020 0 |
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10.1016/j.biocel.2020.105820 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001117.pica (DE-627)ELV051206706 (ELSEVIER)S1357-2725(20)30137-0 DE-627 ger DE-627 rakwb eng 610 VZ 610 VZ 44.85 bkl Liu, Jing verfasserin aut Valproic acid overcomes sorafenib resistance by reducing the migration of Jagged2-mediated Notch1 signaling pathway in hepatocellular carcinoma cells 2020transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Sorafenib resistance is a classic problem related to the treatment of advanced hepatocellular carcinoma (HCC). There is a recognized need to explore new drug resistance mechanisms and develop novel strategies to overcome the acquired resistance to sorafenib. Although one study has showed that the anti-epileptic drug valproic acid (VPA) could sensitize transforming growth factor-β (TGF-β)-induced sorafenib-resistant HCC cells, it is unclear whether VPA could reverse resistance to long-term clinical treatment with sorafenib. In this study, we successfully established sorafenib-resistant HCC cells by long-term sorafenib exposure. Compared with sensitive HCC cells, the proliferation, anti-apoptotic capability and migration of the sorafenib-resistant cells were enhanced. In addition, we found that VPA combined with sorafenib could overcome drug resistance by downregulating Jagged2-mediated Notch1 signaling pathway and epithelial-mesenchymal transition (EMT)-related proteins. Furthermore, the combination of VPA and sorafenib could obviously increase the sensitivity of drug-resistant cells in vitro and synergistically suppress tumor growth in vivo. These results provided a new insight that the use of VPA in combination with sorafenib was an effective method for clinically solving the problem of sorafenib resistance by modulating the Jagged2-mediated Notch1 signaling pathway and reversing the EMT phenotype. Sorafenib resistance is a classic problem related to the treatment of advanced hepatocellular carcinoma (HCC). There is a recognized need to explore new drug resistance mechanisms and develop novel strategies to overcome the acquired resistance to sorafenib. Although one study has showed that the anti-epileptic drug valproic acid (VPA) could sensitize transforming growth factor-β (TGF-β)-induced sorafenib-resistant HCC cells, it is unclear whether VPA could reverse resistance to long-term clinical treatment with sorafenib. In this study, we successfully established sorafenib-resistant HCC cells by long-term sorafenib exposure. Compared with sensitive HCC cells, the proliferation, anti-apoptotic capability and migration of the sorafenib-resistant cells were enhanced. In addition, we found that VPA combined with sorafenib could overcome drug resistance by downregulating Jagged2-mediated Notch1 signaling pathway and epithelial-mesenchymal transition (EMT)-related proteins. Furthermore, the combination of VPA and sorafenib could obviously increase the sensitivity of drug-resistant cells in vitro and synergistically suppress tumor growth in vivo. These results provided a new insight that the use of VPA in combination with sorafenib was an effective method for clinically solving the problem of sorafenib resistance by modulating the Jagged2-mediated Notch1 signaling pathway and reversing the EMT phenotype. Jagged2 Elsevier Notch1 Elsevier Migration Elsevier Sorafenib resistance Elsevier Valproic acid Elsevier Yang, Xu oth Liang, Qing oth Yu, Yan oth Shen, Xiaoying oth Sun, Guangchun oth Enthalten in Elsevier Urological Diseases of the Byzantine Emperors (330-1453) 2011 Amsterdam (DE-627)ELV010616845 volume:126 year:2020 pages:0 https://doi.org/10.1016/j.biocel.2020.105820 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 44.85 Kardiologie Angiologie VZ AR 126 2020 0 |
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10.1016/j.biocel.2020.105820 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001117.pica (DE-627)ELV051206706 (ELSEVIER)S1357-2725(20)30137-0 DE-627 ger DE-627 rakwb eng 610 VZ 610 VZ 44.85 bkl Liu, Jing verfasserin aut Valproic acid overcomes sorafenib resistance by reducing the migration of Jagged2-mediated Notch1 signaling pathway in hepatocellular carcinoma cells 2020transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Sorafenib resistance is a classic problem related to the treatment of advanced hepatocellular carcinoma (HCC). There is a recognized need to explore new drug resistance mechanisms and develop novel strategies to overcome the acquired resistance to sorafenib. Although one study has showed that the anti-epileptic drug valproic acid (VPA) could sensitize transforming growth factor-β (TGF-β)-induced sorafenib-resistant HCC cells, it is unclear whether VPA could reverse resistance to long-term clinical treatment with sorafenib. In this study, we successfully established sorafenib-resistant HCC cells by long-term sorafenib exposure. Compared with sensitive HCC cells, the proliferation, anti-apoptotic capability and migration of the sorafenib-resistant cells were enhanced. In addition, we found that VPA combined with sorafenib could overcome drug resistance by downregulating Jagged2-mediated Notch1 signaling pathway and epithelial-mesenchymal transition (EMT)-related proteins. Furthermore, the combination of VPA and sorafenib could obviously increase the sensitivity of drug-resistant cells in vitro and synergistically suppress tumor growth in vivo. These results provided a new insight that the use of VPA in combination with sorafenib was an effective method for clinically solving the problem of sorafenib resistance by modulating the Jagged2-mediated Notch1 signaling pathway and reversing the EMT phenotype. Sorafenib resistance is a classic problem related to the treatment of advanced hepatocellular carcinoma (HCC). There is a recognized need to explore new drug resistance mechanisms and develop novel strategies to overcome the acquired resistance to sorafenib. Although one study has showed that the anti-epileptic drug valproic acid (VPA) could sensitize transforming growth factor-β (TGF-β)-induced sorafenib-resistant HCC cells, it is unclear whether VPA could reverse resistance to long-term clinical treatment with sorafenib. In this study, we successfully established sorafenib-resistant HCC cells by long-term sorafenib exposure. Compared with sensitive HCC cells, the proliferation, anti-apoptotic capability and migration of the sorafenib-resistant cells were enhanced. In addition, we found that VPA combined with sorafenib could overcome drug resistance by downregulating Jagged2-mediated Notch1 signaling pathway and epithelial-mesenchymal transition (EMT)-related proteins. Furthermore, the combination of VPA and sorafenib could obviously increase the sensitivity of drug-resistant cells in vitro and synergistically suppress tumor growth in vivo. These results provided a new insight that the use of VPA in combination with sorafenib was an effective method for clinically solving the problem of sorafenib resistance by modulating the Jagged2-mediated Notch1 signaling pathway and reversing the EMT phenotype. Jagged2 Elsevier Notch1 Elsevier Migration Elsevier Sorafenib resistance Elsevier Valproic acid Elsevier Yang, Xu oth Liang, Qing oth Yu, Yan oth Shen, Xiaoying oth Sun, Guangchun oth Enthalten in Elsevier Urological Diseases of the Byzantine Emperors (330-1453) 2011 Amsterdam (DE-627)ELV010616845 volume:126 year:2020 pages:0 https://doi.org/10.1016/j.biocel.2020.105820 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA 44.85 Kardiologie Angiologie VZ AR 126 2020 0 |
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Valproic acid overcomes sorafenib resistance by reducing the migration of Jagged2-mediated Notch1 signaling pathway in hepatocellular carcinoma cells |
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Sorafenib resistance is a classic problem related to the treatment of advanced hepatocellular carcinoma (HCC). There is a recognized need to explore new drug resistance mechanisms and develop novel strategies to overcome the acquired resistance to sorafenib. Although one study has showed that the anti-epileptic drug valproic acid (VPA) could sensitize transforming growth factor-β (TGF-β)-induced sorafenib-resistant HCC cells, it is unclear whether VPA could reverse resistance to long-term clinical treatment with sorafenib. In this study, we successfully established sorafenib-resistant HCC cells by long-term sorafenib exposure. Compared with sensitive HCC cells, the proliferation, anti-apoptotic capability and migration of the sorafenib-resistant cells were enhanced. In addition, we found that VPA combined with sorafenib could overcome drug resistance by downregulating Jagged2-mediated Notch1 signaling pathway and epithelial-mesenchymal transition (EMT)-related proteins. Furthermore, the combination of VPA and sorafenib could obviously increase the sensitivity of drug-resistant cells in vitro and synergistically suppress tumor growth in vivo. These results provided a new insight that the use of VPA in combination with sorafenib was an effective method for clinically solving the problem of sorafenib resistance by modulating the Jagged2-mediated Notch1 signaling pathway and reversing the EMT phenotype. |
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Sorafenib resistance is a classic problem related to the treatment of advanced hepatocellular carcinoma (HCC). There is a recognized need to explore new drug resistance mechanisms and develop novel strategies to overcome the acquired resistance to sorafenib. Although one study has showed that the anti-epileptic drug valproic acid (VPA) could sensitize transforming growth factor-β (TGF-β)-induced sorafenib-resistant HCC cells, it is unclear whether VPA could reverse resistance to long-term clinical treatment with sorafenib. In this study, we successfully established sorafenib-resistant HCC cells by long-term sorafenib exposure. Compared with sensitive HCC cells, the proliferation, anti-apoptotic capability and migration of the sorafenib-resistant cells were enhanced. In addition, we found that VPA combined with sorafenib could overcome drug resistance by downregulating Jagged2-mediated Notch1 signaling pathway and epithelial-mesenchymal transition (EMT)-related proteins. Furthermore, the combination of VPA and sorafenib could obviously increase the sensitivity of drug-resistant cells in vitro and synergistically suppress tumor growth in vivo. These results provided a new insight that the use of VPA in combination with sorafenib was an effective method for clinically solving the problem of sorafenib resistance by modulating the Jagged2-mediated Notch1 signaling pathway and reversing the EMT phenotype. |
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Sorafenib resistance is a classic problem related to the treatment of advanced hepatocellular carcinoma (HCC). There is a recognized need to explore new drug resistance mechanisms and develop novel strategies to overcome the acquired resistance to sorafenib. Although one study has showed that the anti-epileptic drug valproic acid (VPA) could sensitize transforming growth factor-β (TGF-β)-induced sorafenib-resistant HCC cells, it is unclear whether VPA could reverse resistance to long-term clinical treatment with sorafenib. In this study, we successfully established sorafenib-resistant HCC cells by long-term sorafenib exposure. Compared with sensitive HCC cells, the proliferation, anti-apoptotic capability and migration of the sorafenib-resistant cells were enhanced. In addition, we found that VPA combined with sorafenib could overcome drug resistance by downregulating Jagged2-mediated Notch1 signaling pathway and epithelial-mesenchymal transition (EMT)-related proteins. Furthermore, the combination of VPA and sorafenib could obviously increase the sensitivity of drug-resistant cells in vitro and synergistically suppress tumor growth in vivo. These results provided a new insight that the use of VPA in combination with sorafenib was an effective method for clinically solving the problem of sorafenib resistance by modulating the Jagged2-mediated Notch1 signaling pathway and reversing the EMT phenotype. |
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