FTY720 inhibits the Nrf2/ARE pathway in human glioblastoma cell lines and sensitizes glioblastoma cells to temozolomide
Background Nuclear factor erythroid 2-related factor 2 (Nrf2) is a redox-sensitive transcription factor regulating the expression of various cytoprotective genes. Constitutive Nrf2 activation in many cancers enhances cell survival and resistance to anti-cancer drugs. Our previous studies have shown...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Zhang, Li [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2017 |
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| Anmerkung: |
© Maj Institute of Pharmacology, Polish Academy of Sciences 2017 |
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| Übergeordnetes Werk: |
Enthalten in: Pharmacological reports - Heidelberg : Springer Nature, 1998, 69(2017), 6 vom: 04. Juli, Seite 1186-1193 |
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| Übergeordnetes Werk: |
volume:69 ; year:2017 ; number:6 ; day:04 ; month:07 ; pages:1186-1193 |
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| DOI / URN: |
10.1016/j.pharep.2017.07.003 |
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| Katalog-ID: |
SPR038900246 |
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| 100 | 1 | |a Zhang, Li |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a FTY720 inhibits the Nrf2/ARE pathway in human glioblastoma cell lines and sensitizes glioblastoma cells to temozolomide |
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| 520 | |a Background Nuclear factor erythroid 2-related factor 2 (Nrf2) is a redox-sensitive transcription factor regulating the expression of various cytoprotective genes. Constitutive Nrf2 activation in many cancers enhances cell survival and resistance to anti-cancer drugs. Our previous studies have shown that FTY720 induced autophagy-related apoptosis and necroptosis and inhibited invasion and migration in human glioblastoma cells. However, whether FTY720 regulated Nrf2 in glioblastoma cells remained unclear. Methods Cell viability assay, western blot, migration and invasion assay, short hairpin RNA (shRNA) were used. Results We found that FTY720 suppressed the protein and mRNA levels of Nrf2 in human U251MG and U87MG glioblastoma cells lines. In addition, the protein and mRNA levels of heme oxygenase-1 (HO-1) and NADPH:quinine oxidoreductase-1 (NQO-1), two representative target factors of Nrf2, also decreased upon FTY720 treatment. Knockdown of Nrf2 further promoted the anti-cancer effects of FTY720, while activation of Nrf2 exist the opposite effects. In addition, FTY720 significantly sensitized glioblastoma cells to temozolomide (TMZ). However, activation of Nrf2 essentially abolished the induced sensitivity by FTY720. Conclusion Our results indicated the potential application of FTY720 in treatment of glioblastoma and demonstrated that inhibition of Nrf2 can enhance the sensitivity of cancer cells to chemotherapeutic drugs. | ||
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| 650 | 4 | |a TMZ |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Combination chemotherapy |7 (dpeaa)DE-He213 | |
| 700 | 1 | |a Wang, Handong |4 aut | |
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10.1016/j.pharep.2017.07.003 doi (DE-627)SPR038900246 (SPR)j.pharep.2017.07.003-e DE-627 ger DE-627 rakwb eng Zhang, Li verfasserin aut FTY720 inhibits the Nrf2/ARE pathway in human glioblastoma cell lines and sensitizes glioblastoma cells to temozolomide 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Maj Institute of Pharmacology, Polish Academy of Sciences 2017 Background Nuclear factor erythroid 2-related factor 2 (Nrf2) is a redox-sensitive transcription factor regulating the expression of various cytoprotective genes. Constitutive Nrf2 activation in many cancers enhances cell survival and resistance to anti-cancer drugs. Our previous studies have shown that FTY720 induced autophagy-related apoptosis and necroptosis and inhibited invasion and migration in human glioblastoma cells. However, whether FTY720 regulated Nrf2 in glioblastoma cells remained unclear. Methods Cell viability assay, western blot, migration and invasion assay, short hairpin RNA (shRNA) were used. Results We found that FTY720 suppressed the protein and mRNA levels of Nrf2 in human U251MG and U87MG glioblastoma cells lines. In addition, the protein and mRNA levels of heme oxygenase-1 (HO-1) and NADPH:quinine oxidoreductase-1 (NQO-1), two representative target factors of Nrf2, also decreased upon FTY720 treatment. Knockdown of Nrf2 further promoted the anti-cancer effects of FTY720, while activation of Nrf2 exist the opposite effects. In addition, FTY720 significantly sensitized glioblastoma cells to temozolomide (TMZ). However, activation of Nrf2 essentially abolished the induced sensitivity by FTY720. Conclusion Our results indicated the potential application of FTY720 in treatment of glioblastoma and demonstrated that inhibition of Nrf2 can enhance the sensitivity of cancer cells to chemotherapeutic drugs. FTY720 (dpeaa)DE-He213 Glioblastoma (dpeaa)DE-He213 Nrf2 (dpeaa)DE-He213 TMZ (dpeaa)DE-He213 Combination chemotherapy (dpeaa)DE-He213 Wang, Handong aut Enthalten in Pharmacological reports Heidelberg : Springer Nature, 1998 69(2017), 6 vom: 04. Juli, Seite 1186-1193 (DE-627)375964215 (DE-600)2129019-2 2299-5684 nnns volume:69 year:2017 number:6 day:04 month:07 pages:1186-1193 https://dx.doi.org/10.1016/j.pharep.2017.07.003 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_647 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2098 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 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_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 69 2017 6 04 07 1186-1193 |
| spelling |
10.1016/j.pharep.2017.07.003 doi (DE-627)SPR038900246 (SPR)j.pharep.2017.07.003-e DE-627 ger DE-627 rakwb eng Zhang, Li verfasserin aut FTY720 inhibits the Nrf2/ARE pathway in human glioblastoma cell lines and sensitizes glioblastoma cells to temozolomide 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Maj Institute of Pharmacology, Polish Academy of Sciences 2017 Background Nuclear factor erythroid 2-related factor 2 (Nrf2) is a redox-sensitive transcription factor regulating the expression of various cytoprotective genes. Constitutive Nrf2 activation in many cancers enhances cell survival and resistance to anti-cancer drugs. Our previous studies have shown that FTY720 induced autophagy-related apoptosis and necroptosis and inhibited invasion and migration in human glioblastoma cells. However, whether FTY720 regulated Nrf2 in glioblastoma cells remained unclear. Methods Cell viability assay, western blot, migration and invasion assay, short hairpin RNA (shRNA) were used. Results We found that FTY720 suppressed the protein and mRNA levels of Nrf2 in human U251MG and U87MG glioblastoma cells lines. In addition, the protein and mRNA levels of heme oxygenase-1 (HO-1) and NADPH:quinine oxidoreductase-1 (NQO-1), two representative target factors of Nrf2, also decreased upon FTY720 treatment. Knockdown of Nrf2 further promoted the anti-cancer effects of FTY720, while activation of Nrf2 exist the opposite effects. In addition, FTY720 significantly sensitized glioblastoma cells to temozolomide (TMZ). However, activation of Nrf2 essentially abolished the induced sensitivity by FTY720. Conclusion Our results indicated the potential application of FTY720 in treatment of glioblastoma and demonstrated that inhibition of Nrf2 can enhance the sensitivity of cancer cells to chemotherapeutic drugs. FTY720 (dpeaa)DE-He213 Glioblastoma (dpeaa)DE-He213 Nrf2 (dpeaa)DE-He213 TMZ (dpeaa)DE-He213 Combination chemotherapy (dpeaa)DE-He213 Wang, Handong aut Enthalten in Pharmacological reports Heidelberg : Springer Nature, 1998 69(2017), 6 vom: 04. Juli, Seite 1186-1193 (DE-627)375964215 (DE-600)2129019-2 2299-5684 nnns volume:69 year:2017 number:6 day:04 month:07 pages:1186-1193 https://dx.doi.org/10.1016/j.pharep.2017.07.003 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_647 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2098 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 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_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 69 2017 6 04 07 1186-1193 |
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10.1016/j.pharep.2017.07.003 doi (DE-627)SPR038900246 (SPR)j.pharep.2017.07.003-e DE-627 ger DE-627 rakwb eng Zhang, Li verfasserin aut FTY720 inhibits the Nrf2/ARE pathway in human glioblastoma cell lines and sensitizes glioblastoma cells to temozolomide 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Maj Institute of Pharmacology, Polish Academy of Sciences 2017 Background Nuclear factor erythroid 2-related factor 2 (Nrf2) is a redox-sensitive transcription factor regulating the expression of various cytoprotective genes. Constitutive Nrf2 activation in many cancers enhances cell survival and resistance to anti-cancer drugs. Our previous studies have shown that FTY720 induced autophagy-related apoptosis and necroptosis and inhibited invasion and migration in human glioblastoma cells. However, whether FTY720 regulated Nrf2 in glioblastoma cells remained unclear. Methods Cell viability assay, western blot, migration and invasion assay, short hairpin RNA (shRNA) were used. Results We found that FTY720 suppressed the protein and mRNA levels of Nrf2 in human U251MG and U87MG glioblastoma cells lines. In addition, the protein and mRNA levels of heme oxygenase-1 (HO-1) and NADPH:quinine oxidoreductase-1 (NQO-1), two representative target factors of Nrf2, also decreased upon FTY720 treatment. Knockdown of Nrf2 further promoted the anti-cancer effects of FTY720, while activation of Nrf2 exist the opposite effects. In addition, FTY720 significantly sensitized glioblastoma cells to temozolomide (TMZ). However, activation of Nrf2 essentially abolished the induced sensitivity by FTY720. Conclusion Our results indicated the potential application of FTY720 in treatment of glioblastoma and demonstrated that inhibition of Nrf2 can enhance the sensitivity of cancer cells to chemotherapeutic drugs. FTY720 (dpeaa)DE-He213 Glioblastoma (dpeaa)DE-He213 Nrf2 (dpeaa)DE-He213 TMZ (dpeaa)DE-He213 Combination chemotherapy (dpeaa)DE-He213 Wang, Handong aut Enthalten in Pharmacological reports Heidelberg : Springer Nature, 1998 69(2017), 6 vom: 04. Juli, Seite 1186-1193 (DE-627)375964215 (DE-600)2129019-2 2299-5684 nnns volume:69 year:2017 number:6 day:04 month:07 pages:1186-1193 https://dx.doi.org/10.1016/j.pharep.2017.07.003 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_647 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2098 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 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_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 69 2017 6 04 07 1186-1193 |
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10.1016/j.pharep.2017.07.003 doi (DE-627)SPR038900246 (SPR)j.pharep.2017.07.003-e DE-627 ger DE-627 rakwb eng Zhang, Li verfasserin aut FTY720 inhibits the Nrf2/ARE pathway in human glioblastoma cell lines and sensitizes glioblastoma cells to temozolomide 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Maj Institute of Pharmacology, Polish Academy of Sciences 2017 Background Nuclear factor erythroid 2-related factor 2 (Nrf2) is a redox-sensitive transcription factor regulating the expression of various cytoprotective genes. Constitutive Nrf2 activation in many cancers enhances cell survival and resistance to anti-cancer drugs. Our previous studies have shown that FTY720 induced autophagy-related apoptosis and necroptosis and inhibited invasion and migration in human glioblastoma cells. However, whether FTY720 regulated Nrf2 in glioblastoma cells remained unclear. Methods Cell viability assay, western blot, migration and invasion assay, short hairpin RNA (shRNA) were used. Results We found that FTY720 suppressed the protein and mRNA levels of Nrf2 in human U251MG and U87MG glioblastoma cells lines. In addition, the protein and mRNA levels of heme oxygenase-1 (HO-1) and NADPH:quinine oxidoreductase-1 (NQO-1), two representative target factors of Nrf2, also decreased upon FTY720 treatment. Knockdown of Nrf2 further promoted the anti-cancer effects of FTY720, while activation of Nrf2 exist the opposite effects. In addition, FTY720 significantly sensitized glioblastoma cells to temozolomide (TMZ). However, activation of Nrf2 essentially abolished the induced sensitivity by FTY720. Conclusion Our results indicated the potential application of FTY720 in treatment of glioblastoma and demonstrated that inhibition of Nrf2 can enhance the sensitivity of cancer cells to chemotherapeutic drugs. FTY720 (dpeaa)DE-He213 Glioblastoma (dpeaa)DE-He213 Nrf2 (dpeaa)DE-He213 TMZ (dpeaa)DE-He213 Combination chemotherapy (dpeaa)DE-He213 Wang, Handong aut Enthalten in Pharmacological reports Heidelberg : Springer Nature, 1998 69(2017), 6 vom: 04. Juli, Seite 1186-1193 (DE-627)375964215 (DE-600)2129019-2 2299-5684 nnns volume:69 year:2017 number:6 day:04 month:07 pages:1186-1193 https://dx.doi.org/10.1016/j.pharep.2017.07.003 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_647 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2098 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 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_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 69 2017 6 04 07 1186-1193 |
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10.1016/j.pharep.2017.07.003 doi (DE-627)SPR038900246 (SPR)j.pharep.2017.07.003-e DE-627 ger DE-627 rakwb eng Zhang, Li verfasserin aut FTY720 inhibits the Nrf2/ARE pathway in human glioblastoma cell lines and sensitizes glioblastoma cells to temozolomide 2017 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Maj Institute of Pharmacology, Polish Academy of Sciences 2017 Background Nuclear factor erythroid 2-related factor 2 (Nrf2) is a redox-sensitive transcription factor regulating the expression of various cytoprotective genes. Constitutive Nrf2 activation in many cancers enhances cell survival and resistance to anti-cancer drugs. Our previous studies have shown that FTY720 induced autophagy-related apoptosis and necroptosis and inhibited invasion and migration in human glioblastoma cells. However, whether FTY720 regulated Nrf2 in glioblastoma cells remained unclear. Methods Cell viability assay, western blot, migration and invasion assay, short hairpin RNA (shRNA) were used. Results We found that FTY720 suppressed the protein and mRNA levels of Nrf2 in human U251MG and U87MG glioblastoma cells lines. In addition, the protein and mRNA levels of heme oxygenase-1 (HO-1) and NADPH:quinine oxidoreductase-1 (NQO-1), two representative target factors of Nrf2, also decreased upon FTY720 treatment. Knockdown of Nrf2 further promoted the anti-cancer effects of FTY720, while activation of Nrf2 exist the opposite effects. In addition, FTY720 significantly sensitized glioblastoma cells to temozolomide (TMZ). However, activation of Nrf2 essentially abolished the induced sensitivity by FTY720. Conclusion Our results indicated the potential application of FTY720 in treatment of glioblastoma and demonstrated that inhibition of Nrf2 can enhance the sensitivity of cancer cells to chemotherapeutic drugs. FTY720 (dpeaa)DE-He213 Glioblastoma (dpeaa)DE-He213 Nrf2 (dpeaa)DE-He213 TMZ (dpeaa)DE-He213 Combination chemotherapy (dpeaa)DE-He213 Wang, Handong aut Enthalten in Pharmacological reports Heidelberg : Springer Nature, 1998 69(2017), 6 vom: 04. Juli, Seite 1186-1193 (DE-627)375964215 (DE-600)2129019-2 2299-5684 nnns volume:69 year:2017 number:6 day:04 month:07 pages:1186-1193 https://dx.doi.org/10.1016/j.pharep.2017.07.003 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_647 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2098 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 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_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 69 2017 6 04 07 1186-1193 |
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Constitutive Nrf2 activation in many cancers enhances cell survival and resistance to anti-cancer drugs. Our previous studies have shown that FTY720 induced autophagy-related apoptosis and necroptosis and inhibited invasion and migration in human glioblastoma cells. However, whether FTY720 regulated Nrf2 in glioblastoma cells remained unclear. Methods Cell viability assay, western blot, migration and invasion assay, short hairpin RNA (shRNA) were used. Results We found that FTY720 suppressed the protein and mRNA levels of Nrf2 in human U251MG and U87MG glioblastoma cells lines. In addition, the protein and mRNA levels of heme oxygenase-1 (HO-1) and NADPH:quinine oxidoreductase-1 (NQO-1), two representative target factors of Nrf2, also decreased upon FTY720 treatment. Knockdown of Nrf2 further promoted the anti-cancer effects of FTY720, while activation of Nrf2 exist the opposite effects. In addition, FTY720 significantly sensitized glioblastoma cells to temozolomide (TMZ). However, activation of Nrf2 essentially abolished the induced sensitivity by FTY720. 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Zhang, Li |
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Zhang, Li misc FTY720 misc Glioblastoma misc Nrf2 misc TMZ misc Combination chemotherapy FTY720 inhibits the Nrf2/ARE pathway in human glioblastoma cell lines and sensitizes glioblastoma cells to temozolomide |
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FTY720 inhibits the Nrf2/ARE pathway in human glioblastoma cell lines and sensitizes glioblastoma cells to temozolomide FTY720 (dpeaa)DE-He213 Glioblastoma (dpeaa)DE-He213 Nrf2 (dpeaa)DE-He213 TMZ (dpeaa)DE-He213 Combination chemotherapy (dpeaa)DE-He213 |
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FTY720 inhibits the Nrf2/ARE pathway in human glioblastoma cell lines and sensitizes glioblastoma cells to temozolomide |
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FTY720 inhibits the Nrf2/ARE pathway in human glioblastoma cell lines and sensitizes glioblastoma cells to temozolomide |
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fty720 inhibits the nrf2/are pathway in human glioblastoma cell lines and sensitizes glioblastoma cells to temozolomide |
| title_auth |
FTY720 inhibits the Nrf2/ARE pathway in human glioblastoma cell lines and sensitizes glioblastoma cells to temozolomide |
| abstract |
Background Nuclear factor erythroid 2-related factor 2 (Nrf2) is a redox-sensitive transcription factor regulating the expression of various cytoprotective genes. Constitutive Nrf2 activation in many cancers enhances cell survival and resistance to anti-cancer drugs. Our previous studies have shown that FTY720 induced autophagy-related apoptosis and necroptosis and inhibited invasion and migration in human glioblastoma cells. However, whether FTY720 regulated Nrf2 in glioblastoma cells remained unclear. Methods Cell viability assay, western blot, migration and invasion assay, short hairpin RNA (shRNA) were used. Results We found that FTY720 suppressed the protein and mRNA levels of Nrf2 in human U251MG and U87MG glioblastoma cells lines. In addition, the protein and mRNA levels of heme oxygenase-1 (HO-1) and NADPH:quinine oxidoreductase-1 (NQO-1), two representative target factors of Nrf2, also decreased upon FTY720 treatment. Knockdown of Nrf2 further promoted the anti-cancer effects of FTY720, while activation of Nrf2 exist the opposite effects. In addition, FTY720 significantly sensitized glioblastoma cells to temozolomide (TMZ). However, activation of Nrf2 essentially abolished the induced sensitivity by FTY720. Conclusion Our results indicated the potential application of FTY720 in treatment of glioblastoma and demonstrated that inhibition of Nrf2 can enhance the sensitivity of cancer cells to chemotherapeutic drugs. © Maj Institute of Pharmacology, Polish Academy of Sciences 2017 |
| abstractGer |
Background Nuclear factor erythroid 2-related factor 2 (Nrf2) is a redox-sensitive transcription factor regulating the expression of various cytoprotective genes. Constitutive Nrf2 activation in many cancers enhances cell survival and resistance to anti-cancer drugs. Our previous studies have shown that FTY720 induced autophagy-related apoptosis and necroptosis and inhibited invasion and migration in human glioblastoma cells. However, whether FTY720 regulated Nrf2 in glioblastoma cells remained unclear. Methods Cell viability assay, western blot, migration and invasion assay, short hairpin RNA (shRNA) were used. Results We found that FTY720 suppressed the protein and mRNA levels of Nrf2 in human U251MG and U87MG glioblastoma cells lines. In addition, the protein and mRNA levels of heme oxygenase-1 (HO-1) and NADPH:quinine oxidoreductase-1 (NQO-1), two representative target factors of Nrf2, also decreased upon FTY720 treatment. Knockdown of Nrf2 further promoted the anti-cancer effects of FTY720, while activation of Nrf2 exist the opposite effects. In addition, FTY720 significantly sensitized glioblastoma cells to temozolomide (TMZ). However, activation of Nrf2 essentially abolished the induced sensitivity by FTY720. Conclusion Our results indicated the potential application of FTY720 in treatment of glioblastoma and demonstrated that inhibition of Nrf2 can enhance the sensitivity of cancer cells to chemotherapeutic drugs. © Maj Institute of Pharmacology, Polish Academy of Sciences 2017 |
| abstract_unstemmed |
Background Nuclear factor erythroid 2-related factor 2 (Nrf2) is a redox-sensitive transcription factor regulating the expression of various cytoprotective genes. Constitutive Nrf2 activation in many cancers enhances cell survival and resistance to anti-cancer drugs. Our previous studies have shown that FTY720 induced autophagy-related apoptosis and necroptosis and inhibited invasion and migration in human glioblastoma cells. However, whether FTY720 regulated Nrf2 in glioblastoma cells remained unclear. Methods Cell viability assay, western blot, migration and invasion assay, short hairpin RNA (shRNA) were used. Results We found that FTY720 suppressed the protein and mRNA levels of Nrf2 in human U251MG and U87MG glioblastoma cells lines. In addition, the protein and mRNA levels of heme oxygenase-1 (HO-1) and NADPH:quinine oxidoreductase-1 (NQO-1), two representative target factors of Nrf2, also decreased upon FTY720 treatment. Knockdown of Nrf2 further promoted the anti-cancer effects of FTY720, while activation of Nrf2 exist the opposite effects. In addition, FTY720 significantly sensitized glioblastoma cells to temozolomide (TMZ). However, activation of Nrf2 essentially abolished the induced sensitivity by FTY720. Conclusion Our results indicated the potential application of FTY720 in treatment of glioblastoma and demonstrated that inhibition of Nrf2 can enhance the sensitivity of cancer cells to chemotherapeutic drugs. © Maj Institute of Pharmacology, Polish Academy of Sciences 2017 |
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FTY720 inhibits the Nrf2/ARE pathway in human glioblastoma cell lines and sensitizes glioblastoma cells to temozolomide |
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https://dx.doi.org/10.1016/j.pharep.2017.07.003 |
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| score |
7.3994675 |