Overexpression of Smac by an Armed Vesicular Stomatitis Virus Overcomes Tumor Resistance
Despite reports of successful clinical cases, many tumors appear to resist infection by oncolytic viruses (OVs). To circumvent this problem, an armed vesicular stomatitis virus was constructed by inserting a transgene to express Smac/DIABLO during virus infection (VSV-S). Endogenous Smac in HeLa cel...
Ausführliche Beschreibung
Autor*in: |
Weike Li [verfasserIn] Ravi Chakra Turaga [verfasserIn] Xin Li [verfasserIn] Malvika Sharma [verfasserIn] Zahra Enadi [verfasserIn] Sydney Nicole Dunham Tompkins [verfasserIn] Kyle Christian Hardy [verfasserIn] Falguni Mishra [verfasserIn] Jun Tsao [verfasserIn] Zhi-ren Liu [verfasserIn] Daping Fan [verfasserIn] Ming Luo [verfasserIn] |
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Format: |
E-Artikel |
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Sprache: |
Englisch |
Erschienen: |
2019 |
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Übergeordnetes Werk: |
In: Molecular Therapy: Oncolytics - Elsevier, 2016, 14(2019), Seite 188-195 |
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Übergeordnetes Werk: |
volume:14 ; year:2019 ; pages:188-195 |
Links: |
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DOI / URN: |
10.1016/j.omto.2019.05.006 |
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Katalog-ID: |
DOAJ070572151 |
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10.1016/j.omto.2019.05.006 doi (DE-627)DOAJ070572151 (DE-599)DOAJ01e6204ec62e4f168d3f98b030c1a988 DE-627 ger DE-627 rakwb eng RC254-282 Weike Li verfasserin aut Overexpression of Smac by an Armed Vesicular Stomatitis Virus Overcomes Tumor Resistance 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Despite reports of successful clinical cases, many tumors appear to resist infection by oncolytic viruses (OVs). To circumvent this problem, an armed vesicular stomatitis virus was constructed by inserting a transgene to express Smac/DIABLO during virus infection (VSV-S). Endogenous Smac in HeLa cells was diminished during wtVSV infection, whereas the Smac level was enhanced during VSV-S infection. Apoptosis was readily induced by VSV-S, but not wtVSV, infection. More importantly, the tumor volume was reduced to a larger extent when xenografts of 4T1 cells in BALB/c mice and OV-resistant T-47D cells in nude mice were intratumorally injected with VSV-S. VSV-S represents a novel mechanism to overcome tumor resistance, resulting in more significant tumor regression due to enhanced apoptosis. Neoplasms. Tumors. Oncology. Including cancer and carcinogens Ravi Chakra Turaga verfasserin aut Xin Li verfasserin aut Malvika Sharma verfasserin aut Zahra Enadi verfasserin aut Sydney Nicole Dunham Tompkins verfasserin aut Kyle Christian Hardy verfasserin aut Falguni Mishra verfasserin aut Jun Tsao verfasserin aut Zhi-ren Liu verfasserin aut Daping Fan verfasserin aut Ming Luo verfasserin aut In Molecular Therapy: Oncolytics Elsevier, 2016 14(2019), Seite 188-195 (DE-627)843857420 (DE-600)2842549-2 23727705 nnns volume:14 year:2019 pages:188-195 https://doi.org/10.1016/j.omto.2019.05.006 kostenfrei https://doaj.org/article/01e6204ec62e4f168d3f98b030c1a988 kostenfrei http://www.sciencedirect.com/science/article/pii/S2372770519300622 kostenfrei https://doaj.org/toc/2372-7705 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 14 2019 188-195 |
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10.1016/j.omto.2019.05.006 doi (DE-627)DOAJ070572151 (DE-599)DOAJ01e6204ec62e4f168d3f98b030c1a988 DE-627 ger DE-627 rakwb eng RC254-282 Weike Li verfasserin aut Overexpression of Smac by an Armed Vesicular Stomatitis Virus Overcomes Tumor Resistance 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Despite reports of successful clinical cases, many tumors appear to resist infection by oncolytic viruses (OVs). To circumvent this problem, an armed vesicular stomatitis virus was constructed by inserting a transgene to express Smac/DIABLO during virus infection (VSV-S). Endogenous Smac in HeLa cells was diminished during wtVSV infection, whereas the Smac level was enhanced during VSV-S infection. Apoptosis was readily induced by VSV-S, but not wtVSV, infection. More importantly, the tumor volume was reduced to a larger extent when xenografts of 4T1 cells in BALB/c mice and OV-resistant T-47D cells in nude mice were intratumorally injected with VSV-S. VSV-S represents a novel mechanism to overcome tumor resistance, resulting in more significant tumor regression due to enhanced apoptosis. Neoplasms. Tumors. Oncology. Including cancer and carcinogens Ravi Chakra Turaga verfasserin aut Xin Li verfasserin aut Malvika Sharma verfasserin aut Zahra Enadi verfasserin aut Sydney Nicole Dunham Tompkins verfasserin aut Kyle Christian Hardy verfasserin aut Falguni Mishra verfasserin aut Jun Tsao verfasserin aut Zhi-ren Liu verfasserin aut Daping Fan verfasserin aut Ming Luo verfasserin aut In Molecular Therapy: Oncolytics Elsevier, 2016 14(2019), Seite 188-195 (DE-627)843857420 (DE-600)2842549-2 23727705 nnns volume:14 year:2019 pages:188-195 https://doi.org/10.1016/j.omto.2019.05.006 kostenfrei https://doaj.org/article/01e6204ec62e4f168d3f98b030c1a988 kostenfrei http://www.sciencedirect.com/science/article/pii/S2372770519300622 kostenfrei https://doaj.org/toc/2372-7705 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 14 2019 188-195 |
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Overexpression of Smac by an Armed Vesicular Stomatitis Virus Overcomes Tumor Resistance |
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Despite reports of successful clinical cases, many tumors appear to resist infection by oncolytic viruses (OVs). To circumvent this problem, an armed vesicular stomatitis virus was constructed by inserting a transgene to express Smac/DIABLO during virus infection (VSV-S). Endogenous Smac in HeLa cells was diminished during wtVSV infection, whereas the Smac level was enhanced during VSV-S infection. Apoptosis was readily induced by VSV-S, but not wtVSV, infection. More importantly, the tumor volume was reduced to a larger extent when xenografts of 4T1 cells in BALB/c mice and OV-resistant T-47D cells in nude mice were intratumorally injected with VSV-S. VSV-S represents a novel mechanism to overcome tumor resistance, resulting in more significant tumor regression due to enhanced apoptosis. |
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Despite reports of successful clinical cases, many tumors appear to resist infection by oncolytic viruses (OVs). To circumvent this problem, an armed vesicular stomatitis virus was constructed by inserting a transgene to express Smac/DIABLO during virus infection (VSV-S). Endogenous Smac in HeLa cells was diminished during wtVSV infection, whereas the Smac level was enhanced during VSV-S infection. Apoptosis was readily induced by VSV-S, but not wtVSV, infection. More importantly, the tumor volume was reduced to a larger extent when xenografts of 4T1 cells in BALB/c mice and OV-resistant T-47D cells in nude mice were intratumorally injected with VSV-S. VSV-S represents a novel mechanism to overcome tumor resistance, resulting in more significant tumor regression due to enhanced apoptosis. |
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Despite reports of successful clinical cases, many tumors appear to resist infection by oncolytic viruses (OVs). To circumvent this problem, an armed vesicular stomatitis virus was constructed by inserting a transgene to express Smac/DIABLO during virus infection (VSV-S). Endogenous Smac in HeLa cells was diminished during wtVSV infection, whereas the Smac level was enhanced during VSV-S infection. Apoptosis was readily induced by VSV-S, but not wtVSV, infection. More importantly, the tumor volume was reduced to a larger extent when xenografts of 4T1 cells in BALB/c mice and OV-resistant T-47D cells in nude mice were intratumorally injected with VSV-S. VSV-S represents a novel mechanism to overcome tumor resistance, resulting in more significant tumor regression due to enhanced apoptosis. |
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