ERβ modulates genistein’s cisplatin-enhancing activities in breast cancer MDA-MB-231 cells via P53-independent pathway
Abstract As one of the typical food-derived phytoestrogens, genistein (GEN) could bind to estrogen receptor (ER) and was reported to be closely related to breast cancer. Our former research showed that GEN interfered with the anti-tumor effects of cisplatin (CIS) in breast cancer MCF-7 (ERα+/ERβ−) c...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Liu, Ren [verfasserIn] Xu, Xiaolin [verfasserIn] Liang, Chenglin [verfasserIn] Chen, Xin [verfasserIn] Yu, Xiaowei [verfasserIn] Zhong, Hongfei [verfasserIn] Xu, Wenxiu [verfasserIn] Cheng, Yu [verfasserIn] Wang, Wei [verfasserIn] Wu, Yudong [verfasserIn] Yu, Lehan [verfasserIn] Hu, Xiaojuan [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2019 |
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| Schlagwörter: |
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| Übergeordnetes Werk: |
Enthalten in: Molecular and cellular biochemistry - Dordrecht [u.a.] : Springer Science + Business Media B.V, 1973, 456(2019), 1-2 vom: 08. Feb., Seite 205-216 |
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| Übergeordnetes Werk: |
volume:456 ; year:2019 ; number:1-2 ; day:08 ; month:02 ; pages:205-216 |
| Links: |
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| DOI / URN: |
10.1007/s11010-019-03505-y |
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| Katalog-ID: |
SPR015661202 |
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| 245 | 1 | 0 | |a ERβ modulates genistein’s cisplatin-enhancing activities in breast cancer MDA-MB-231 cells via P53-independent pathway |
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| 520 | |a Abstract As one of the typical food-derived phytoestrogens, genistein (GEN) could bind to estrogen receptor (ER) and was reported to be closely related to breast cancer. Our former research showed that GEN interfered with the anti-tumor effects of cisplatin (CIS) in breast cancer MCF-7 (ERα+/ERβ−) cells. However, it is not clear whether ER expression pattern affects GEN’s modulation on CIS’s activity. In the present study, breast cancer ERβ knockdown (ERβKD) MDA-MB-231 (ERα−/ERβ+) cell model was established via ERβ RNAi lentivirus infection. The role of ERβ expression in GEN’s bioeffects on cells’ response to CIS was investigated and was further double-checked by pathway-specific inhibitor PHTPP. Consistent results were harvested through cell viability analysis, cell cycle distribution flow cytometry, TUNEL staining, and expression detection of key biomarkers, Bax, Bcl-2, P21, P53, and cleaved caspase-3. Compared with the control group, PHTPP-treated or ERβKD cells exhibited higher sensitivity to both GEN and CIS treatment. GEN and CIS showed synergistic effects only in ERβ-deficient cells. This effect mainly resulted in G2 phase arresting and apoptosis induction with the upregulation of P21 and Bax/Bcl-2 protein level. Besides, P53 expression was strikingly suppressed in ERβ-deficient cells. This indicated ERβ pathway deficiency might enhance GEN–CIS bioactivity via the downregulation of P53. In summary, our data imply that daily intake of GEN-rich diet could collaborate with CIS anti-tumor treatment in ERα−/ERβ− breast cancer cases. ERβ pathway might be one of the potential targets which elicit GEN’s positive effects in ERα− breast cancer patients. | ||
| 650 | 4 | |a Genistein |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Cisplatin |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Breast cancer |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a ERβ |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Chemotherapy |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a P53-independent |7 (dpeaa)DE-He213 | |
| 700 | 1 | |a Xu, Xiaolin |e verfasserin |4 aut | |
| 700 | 1 | |a Liang, Chenglin |e verfasserin |4 aut | |
| 700 | 1 | |a Chen, Xin |e verfasserin |4 aut | |
| 700 | 1 | |a Yu, Xiaowei |e verfasserin |4 aut | |
| 700 | 1 | |a Zhong, Hongfei |e verfasserin |4 aut | |
| 700 | 1 | |a Xu, Wenxiu |e verfasserin |4 aut | |
| 700 | 1 | |a Cheng, Yu |e verfasserin |4 aut | |
| 700 | 1 | |a Wang, Wei |e verfasserin |4 aut | |
| 700 | 1 | |a Wu, Yudong |e verfasserin |4 aut | |
| 700 | 1 | |a Yu, Lehan |e verfasserin |4 aut | |
| 700 | 1 | |a Hu, Xiaojuan |e verfasserin |4 aut | |
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10.1007/s11010-019-03505-y doi (DE-627)SPR015661202 (SPR)s11010-019-03505-y-e DE-627 ger DE-627 rakwb eng 540 ASE 44.00 bkl Liu, Ren verfasserin aut ERβ modulates genistein’s cisplatin-enhancing activities in breast cancer MDA-MB-231 cells via P53-independent pathway 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract As one of the typical food-derived phytoestrogens, genistein (GEN) could bind to estrogen receptor (ER) and was reported to be closely related to breast cancer. Our former research showed that GEN interfered with the anti-tumor effects of cisplatin (CIS) in breast cancer MCF-7 (ERα+/ERβ−) cells. However, it is not clear whether ER expression pattern affects GEN’s modulation on CIS’s activity. In the present study, breast cancer ERβ knockdown (ERβKD) MDA-MB-231 (ERα−/ERβ+) cell model was established via ERβ RNAi lentivirus infection. The role of ERβ expression in GEN’s bioeffects on cells’ response to CIS was investigated and was further double-checked by pathway-specific inhibitor PHTPP. Consistent results were harvested through cell viability analysis, cell cycle distribution flow cytometry, TUNEL staining, and expression detection of key biomarkers, Bax, Bcl-2, P21, P53, and cleaved caspase-3. Compared with the control group, PHTPP-treated or ERβKD cells exhibited higher sensitivity to both GEN and CIS treatment. GEN and CIS showed synergistic effects only in ERβ-deficient cells. This effect mainly resulted in G2 phase arresting and apoptosis induction with the upregulation of P21 and Bax/Bcl-2 protein level. Besides, P53 expression was strikingly suppressed in ERβ-deficient cells. This indicated ERβ pathway deficiency might enhance GEN–CIS bioactivity via the downregulation of P53. In summary, our data imply that daily intake of GEN-rich diet could collaborate with CIS anti-tumor treatment in ERα−/ERβ− breast cancer cases. ERβ pathway might be one of the potential targets which elicit GEN’s positive effects in ERα− breast cancer patients. Genistein (dpeaa)DE-He213 Cisplatin (dpeaa)DE-He213 Breast cancer (dpeaa)DE-He213 ERβ (dpeaa)DE-He213 Chemotherapy (dpeaa)DE-He213 P53-independent (dpeaa)DE-He213 Xu, Xiaolin verfasserin aut Liang, Chenglin verfasserin aut Chen, Xin verfasserin aut Yu, Xiaowei verfasserin aut Zhong, Hongfei verfasserin aut Xu, Wenxiu verfasserin aut Cheng, Yu verfasserin aut Wang, Wei verfasserin aut Wu, Yudong verfasserin aut Yu, Lehan verfasserin aut Hu, Xiaojuan verfasserin aut Enthalten in Molecular and cellular biochemistry Dordrecht [u.a.] : Springer Science + Business Media B.V, 1973 456(2019), 1-2 vom: 08. Feb., Seite 205-216 (DE-627)32042975X (DE-600)2003615-2 1573-4919 nnns volume:456 year:2019 number:1-2 day:08 month:02 pages:205-216 https://dx.doi.org/10.1007/s11010-019-03505-y 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_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_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 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_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 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_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_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.00 ASE AR 456 2019 1-2 08 02 205-216 |
| spelling |
10.1007/s11010-019-03505-y doi (DE-627)SPR015661202 (SPR)s11010-019-03505-y-e DE-627 ger DE-627 rakwb eng 540 ASE 44.00 bkl Liu, Ren verfasserin aut ERβ modulates genistein’s cisplatin-enhancing activities in breast cancer MDA-MB-231 cells via P53-independent pathway 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract As one of the typical food-derived phytoestrogens, genistein (GEN) could bind to estrogen receptor (ER) and was reported to be closely related to breast cancer. Our former research showed that GEN interfered with the anti-tumor effects of cisplatin (CIS) in breast cancer MCF-7 (ERα+/ERβ−) cells. However, it is not clear whether ER expression pattern affects GEN’s modulation on CIS’s activity. In the present study, breast cancer ERβ knockdown (ERβKD) MDA-MB-231 (ERα−/ERβ+) cell model was established via ERβ RNAi lentivirus infection. The role of ERβ expression in GEN’s bioeffects on cells’ response to CIS was investigated and was further double-checked by pathway-specific inhibitor PHTPP. Consistent results were harvested through cell viability analysis, cell cycle distribution flow cytometry, TUNEL staining, and expression detection of key biomarkers, Bax, Bcl-2, P21, P53, and cleaved caspase-3. Compared with the control group, PHTPP-treated or ERβKD cells exhibited higher sensitivity to both GEN and CIS treatment. GEN and CIS showed synergistic effects only in ERβ-deficient cells. This effect mainly resulted in G2 phase arresting and apoptosis induction with the upregulation of P21 and Bax/Bcl-2 protein level. Besides, P53 expression was strikingly suppressed in ERβ-deficient cells. This indicated ERβ pathway deficiency might enhance GEN–CIS bioactivity via the downregulation of P53. In summary, our data imply that daily intake of GEN-rich diet could collaborate with CIS anti-tumor treatment in ERα−/ERβ− breast cancer cases. ERβ pathway might be one of the potential targets which elicit GEN’s positive effects in ERα− breast cancer patients. Genistein (dpeaa)DE-He213 Cisplatin (dpeaa)DE-He213 Breast cancer (dpeaa)DE-He213 ERβ (dpeaa)DE-He213 Chemotherapy (dpeaa)DE-He213 P53-independent (dpeaa)DE-He213 Xu, Xiaolin verfasserin aut Liang, Chenglin verfasserin aut Chen, Xin verfasserin aut Yu, Xiaowei verfasserin aut Zhong, Hongfei verfasserin aut Xu, Wenxiu verfasserin aut Cheng, Yu verfasserin aut Wang, Wei verfasserin aut Wu, Yudong verfasserin aut Yu, Lehan verfasserin aut Hu, Xiaojuan verfasserin aut Enthalten in Molecular and cellular biochemistry Dordrecht [u.a.] : Springer Science + Business Media B.V, 1973 456(2019), 1-2 vom: 08. Feb., Seite 205-216 (DE-627)32042975X (DE-600)2003615-2 1573-4919 nnns volume:456 year:2019 number:1-2 day:08 month:02 pages:205-216 https://dx.doi.org/10.1007/s11010-019-03505-y 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_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_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 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_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 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_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_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.00 ASE AR 456 2019 1-2 08 02 205-216 |
| allfields_unstemmed |
10.1007/s11010-019-03505-y doi (DE-627)SPR015661202 (SPR)s11010-019-03505-y-e DE-627 ger DE-627 rakwb eng 540 ASE 44.00 bkl Liu, Ren verfasserin aut ERβ modulates genistein’s cisplatin-enhancing activities in breast cancer MDA-MB-231 cells via P53-independent pathway 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract As one of the typical food-derived phytoestrogens, genistein (GEN) could bind to estrogen receptor (ER) and was reported to be closely related to breast cancer. Our former research showed that GEN interfered with the anti-tumor effects of cisplatin (CIS) in breast cancer MCF-7 (ERα+/ERβ−) cells. However, it is not clear whether ER expression pattern affects GEN’s modulation on CIS’s activity. In the present study, breast cancer ERβ knockdown (ERβKD) MDA-MB-231 (ERα−/ERβ+) cell model was established via ERβ RNAi lentivirus infection. The role of ERβ expression in GEN’s bioeffects on cells’ response to CIS was investigated and was further double-checked by pathway-specific inhibitor PHTPP. Consistent results were harvested through cell viability analysis, cell cycle distribution flow cytometry, TUNEL staining, and expression detection of key biomarkers, Bax, Bcl-2, P21, P53, and cleaved caspase-3. Compared with the control group, PHTPP-treated or ERβKD cells exhibited higher sensitivity to both GEN and CIS treatment. GEN and CIS showed synergistic effects only in ERβ-deficient cells. This effect mainly resulted in G2 phase arresting and apoptosis induction with the upregulation of P21 and Bax/Bcl-2 protein level. Besides, P53 expression was strikingly suppressed in ERβ-deficient cells. This indicated ERβ pathway deficiency might enhance GEN–CIS bioactivity via the downregulation of P53. In summary, our data imply that daily intake of GEN-rich diet could collaborate with CIS anti-tumor treatment in ERα−/ERβ− breast cancer cases. ERβ pathway might be one of the potential targets which elicit GEN’s positive effects in ERα− breast cancer patients. Genistein (dpeaa)DE-He213 Cisplatin (dpeaa)DE-He213 Breast cancer (dpeaa)DE-He213 ERβ (dpeaa)DE-He213 Chemotherapy (dpeaa)DE-He213 P53-independent (dpeaa)DE-He213 Xu, Xiaolin verfasserin aut Liang, Chenglin verfasserin aut Chen, Xin verfasserin aut Yu, Xiaowei verfasserin aut Zhong, Hongfei verfasserin aut Xu, Wenxiu verfasserin aut Cheng, Yu verfasserin aut Wang, Wei verfasserin aut Wu, Yudong verfasserin aut Yu, Lehan verfasserin aut Hu, Xiaojuan verfasserin aut Enthalten in Molecular and cellular biochemistry Dordrecht [u.a.] : Springer Science + Business Media B.V, 1973 456(2019), 1-2 vom: 08. Feb., Seite 205-216 (DE-627)32042975X (DE-600)2003615-2 1573-4919 nnns volume:456 year:2019 number:1-2 day:08 month:02 pages:205-216 https://dx.doi.org/10.1007/s11010-019-03505-y 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_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_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 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_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 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_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_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.00 ASE AR 456 2019 1-2 08 02 205-216 |
| allfieldsGer |
10.1007/s11010-019-03505-y doi (DE-627)SPR015661202 (SPR)s11010-019-03505-y-e DE-627 ger DE-627 rakwb eng 540 ASE 44.00 bkl Liu, Ren verfasserin aut ERβ modulates genistein’s cisplatin-enhancing activities in breast cancer MDA-MB-231 cells via P53-independent pathway 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract As one of the typical food-derived phytoestrogens, genistein (GEN) could bind to estrogen receptor (ER) and was reported to be closely related to breast cancer. Our former research showed that GEN interfered with the anti-tumor effects of cisplatin (CIS) in breast cancer MCF-7 (ERα+/ERβ−) cells. However, it is not clear whether ER expression pattern affects GEN’s modulation on CIS’s activity. In the present study, breast cancer ERβ knockdown (ERβKD) MDA-MB-231 (ERα−/ERβ+) cell model was established via ERβ RNAi lentivirus infection. The role of ERβ expression in GEN’s bioeffects on cells’ response to CIS was investigated and was further double-checked by pathway-specific inhibitor PHTPP. Consistent results were harvested through cell viability analysis, cell cycle distribution flow cytometry, TUNEL staining, and expression detection of key biomarkers, Bax, Bcl-2, P21, P53, and cleaved caspase-3. Compared with the control group, PHTPP-treated or ERβKD cells exhibited higher sensitivity to both GEN and CIS treatment. GEN and CIS showed synergistic effects only in ERβ-deficient cells. This effect mainly resulted in G2 phase arresting and apoptosis induction with the upregulation of P21 and Bax/Bcl-2 protein level. Besides, P53 expression was strikingly suppressed in ERβ-deficient cells. This indicated ERβ pathway deficiency might enhance GEN–CIS bioactivity via the downregulation of P53. In summary, our data imply that daily intake of GEN-rich diet could collaborate with CIS anti-tumor treatment in ERα−/ERβ− breast cancer cases. ERβ pathway might be one of the potential targets which elicit GEN’s positive effects in ERα− breast cancer patients. Genistein (dpeaa)DE-He213 Cisplatin (dpeaa)DE-He213 Breast cancer (dpeaa)DE-He213 ERβ (dpeaa)DE-He213 Chemotherapy (dpeaa)DE-He213 P53-independent (dpeaa)DE-He213 Xu, Xiaolin verfasserin aut Liang, Chenglin verfasserin aut Chen, Xin verfasserin aut Yu, Xiaowei verfasserin aut Zhong, Hongfei verfasserin aut Xu, Wenxiu verfasserin aut Cheng, Yu verfasserin aut Wang, Wei verfasserin aut Wu, Yudong verfasserin aut Yu, Lehan verfasserin aut Hu, Xiaojuan verfasserin aut Enthalten in Molecular and cellular biochemistry Dordrecht [u.a.] : Springer Science + Business Media B.V, 1973 456(2019), 1-2 vom: 08. Feb., Seite 205-216 (DE-627)32042975X (DE-600)2003615-2 1573-4919 nnns volume:456 year:2019 number:1-2 day:08 month:02 pages:205-216 https://dx.doi.org/10.1007/s11010-019-03505-y 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_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_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 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_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 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_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_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.00 ASE AR 456 2019 1-2 08 02 205-216 |
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10.1007/s11010-019-03505-y doi (DE-627)SPR015661202 (SPR)s11010-019-03505-y-e DE-627 ger DE-627 rakwb eng 540 ASE 44.00 bkl Liu, Ren verfasserin aut ERβ modulates genistein’s cisplatin-enhancing activities in breast cancer MDA-MB-231 cells via P53-independent pathway 2019 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract As one of the typical food-derived phytoestrogens, genistein (GEN) could bind to estrogen receptor (ER) and was reported to be closely related to breast cancer. Our former research showed that GEN interfered with the anti-tumor effects of cisplatin (CIS) in breast cancer MCF-7 (ERα+/ERβ−) cells. However, it is not clear whether ER expression pattern affects GEN’s modulation on CIS’s activity. In the present study, breast cancer ERβ knockdown (ERβKD) MDA-MB-231 (ERα−/ERβ+) cell model was established via ERβ RNAi lentivirus infection. The role of ERβ expression in GEN’s bioeffects on cells’ response to CIS was investigated and was further double-checked by pathway-specific inhibitor PHTPP. Consistent results were harvested through cell viability analysis, cell cycle distribution flow cytometry, TUNEL staining, and expression detection of key biomarkers, Bax, Bcl-2, P21, P53, and cleaved caspase-3. Compared with the control group, PHTPP-treated or ERβKD cells exhibited higher sensitivity to both GEN and CIS treatment. GEN and CIS showed synergistic effects only in ERβ-deficient cells. This effect mainly resulted in G2 phase arresting and apoptosis induction with the upregulation of P21 and Bax/Bcl-2 protein level. Besides, P53 expression was strikingly suppressed in ERβ-deficient cells. This indicated ERβ pathway deficiency might enhance GEN–CIS bioactivity via the downregulation of P53. In summary, our data imply that daily intake of GEN-rich diet could collaborate with CIS anti-tumor treatment in ERα−/ERβ− breast cancer cases. ERβ pathway might be one of the potential targets which elicit GEN’s positive effects in ERα− breast cancer patients. Genistein (dpeaa)DE-He213 Cisplatin (dpeaa)DE-He213 Breast cancer (dpeaa)DE-He213 ERβ (dpeaa)DE-He213 Chemotherapy (dpeaa)DE-He213 P53-independent (dpeaa)DE-He213 Xu, Xiaolin verfasserin aut Liang, Chenglin verfasserin aut Chen, Xin verfasserin aut Yu, Xiaowei verfasserin aut Zhong, Hongfei verfasserin aut Xu, Wenxiu verfasserin aut Cheng, Yu verfasserin aut Wang, Wei verfasserin aut Wu, Yudong verfasserin aut Yu, Lehan verfasserin aut Hu, Xiaojuan verfasserin aut Enthalten in Molecular and cellular biochemistry Dordrecht [u.a.] : Springer Science + Business Media B.V, 1973 456(2019), 1-2 vom: 08. Feb., Seite 205-216 (DE-627)32042975X (DE-600)2003615-2 1573-4919 nnns volume:456 year:2019 number:1-2 day:08 month:02 pages:205-216 https://dx.doi.org/10.1007/s11010-019-03505-y 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_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_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 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_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 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_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_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 44.00 ASE AR 456 2019 1-2 08 02 205-216 |
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Enthalten in Molecular and cellular biochemistry 456(2019), 1-2 vom: 08. Feb., Seite 205-216 volume:456 year:2019 number:1-2 day:08 month:02 pages:205-216 |
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Enthalten in Molecular and cellular biochemistry 456(2019), 1-2 vom: 08. Feb., Seite 205-216 volume:456 year:2019 number:1-2 day:08 month:02 pages:205-216 |
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Genistein Cisplatin Breast cancer ERβ Chemotherapy P53-independent |
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Molecular and cellular biochemistry |
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Liu, Ren @@aut@@ Xu, Xiaolin @@aut@@ Liang, Chenglin @@aut@@ Chen, Xin @@aut@@ Yu, Xiaowei @@aut@@ Zhong, Hongfei @@aut@@ Xu, Wenxiu @@aut@@ Cheng, Yu @@aut@@ Wang, Wei @@aut@@ Wu, Yudong @@aut@@ Yu, Lehan @@aut@@ Hu, Xiaojuan @@aut@@ |
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2019-02-08T00:00:00Z |
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Liu, Ren |
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Liu, Ren ddc 540 bkl 44.00 misc Genistein misc Cisplatin misc Breast cancer misc ERβ misc Chemotherapy misc P53-independent ERβ modulates genistein’s cisplatin-enhancing activities in breast cancer MDA-MB-231 cells via P53-independent pathway |
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540 ASE 44.00 bkl ERβ modulates genistein’s cisplatin-enhancing activities in breast cancer MDA-MB-231 cells via P53-independent pathway Genistein (dpeaa)DE-He213 Cisplatin (dpeaa)DE-He213 Breast cancer (dpeaa)DE-He213 ERβ (dpeaa)DE-He213 Chemotherapy (dpeaa)DE-He213 P53-independent (dpeaa)DE-He213 |
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ddc 540 bkl 44.00 misc Genistein misc Cisplatin misc Breast cancer misc ERβ misc Chemotherapy misc P53-independent |
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ddc 540 bkl 44.00 misc Genistein misc Cisplatin misc Breast cancer misc ERβ misc Chemotherapy misc P53-independent |
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ddc 540 bkl 44.00 misc Genistein misc Cisplatin misc Breast cancer misc ERβ misc Chemotherapy misc P53-independent |
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ERβ modulates genistein’s cisplatin-enhancing activities in breast cancer MDA-MB-231 cells via P53-independent pathway |
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ERβ modulates genistein’s cisplatin-enhancing activities in breast cancer MDA-MB-231 cells via P53-independent pathway |
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Molecular and cellular biochemistry |
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Liu, Ren Xu, Xiaolin Liang, Chenglin Chen, Xin Yu, Xiaowei Zhong, Hongfei Xu, Wenxiu Cheng, Yu Wang, Wei Wu, Yudong Yu, Lehan Hu, Xiaojuan |
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erβ modulates genistein’s cisplatin-enhancing activities in breast cancer mda-mb-231 cells via p53-independent pathway |
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ERβ modulates genistein’s cisplatin-enhancing activities in breast cancer MDA-MB-231 cells via P53-independent pathway |
| abstract |
Abstract As one of the typical food-derived phytoestrogens, genistein (GEN) could bind to estrogen receptor (ER) and was reported to be closely related to breast cancer. Our former research showed that GEN interfered with the anti-tumor effects of cisplatin (CIS) in breast cancer MCF-7 (ERα+/ERβ−) cells. However, it is not clear whether ER expression pattern affects GEN’s modulation on CIS’s activity. In the present study, breast cancer ERβ knockdown (ERβKD) MDA-MB-231 (ERα−/ERβ+) cell model was established via ERβ RNAi lentivirus infection. The role of ERβ expression in GEN’s bioeffects on cells’ response to CIS was investigated and was further double-checked by pathway-specific inhibitor PHTPP. Consistent results were harvested through cell viability analysis, cell cycle distribution flow cytometry, TUNEL staining, and expression detection of key biomarkers, Bax, Bcl-2, P21, P53, and cleaved caspase-3. Compared with the control group, PHTPP-treated or ERβKD cells exhibited higher sensitivity to both GEN and CIS treatment. GEN and CIS showed synergistic effects only in ERβ-deficient cells. This effect mainly resulted in G2 phase arresting and apoptosis induction with the upregulation of P21 and Bax/Bcl-2 protein level. Besides, P53 expression was strikingly suppressed in ERβ-deficient cells. This indicated ERβ pathway deficiency might enhance GEN–CIS bioactivity via the downregulation of P53. In summary, our data imply that daily intake of GEN-rich diet could collaborate with CIS anti-tumor treatment in ERα−/ERβ− breast cancer cases. ERβ pathway might be one of the potential targets which elicit GEN’s positive effects in ERα− breast cancer patients. |
| abstractGer |
Abstract As one of the typical food-derived phytoestrogens, genistein (GEN) could bind to estrogen receptor (ER) and was reported to be closely related to breast cancer. Our former research showed that GEN interfered with the anti-tumor effects of cisplatin (CIS) in breast cancer MCF-7 (ERα+/ERβ−) cells. However, it is not clear whether ER expression pattern affects GEN’s modulation on CIS’s activity. In the present study, breast cancer ERβ knockdown (ERβKD) MDA-MB-231 (ERα−/ERβ+) cell model was established via ERβ RNAi lentivirus infection. The role of ERβ expression in GEN’s bioeffects on cells’ response to CIS was investigated and was further double-checked by pathway-specific inhibitor PHTPP. Consistent results were harvested through cell viability analysis, cell cycle distribution flow cytometry, TUNEL staining, and expression detection of key biomarkers, Bax, Bcl-2, P21, P53, and cleaved caspase-3. Compared with the control group, PHTPP-treated or ERβKD cells exhibited higher sensitivity to both GEN and CIS treatment. GEN and CIS showed synergistic effects only in ERβ-deficient cells. This effect mainly resulted in G2 phase arresting and apoptosis induction with the upregulation of P21 and Bax/Bcl-2 protein level. Besides, P53 expression was strikingly suppressed in ERβ-deficient cells. This indicated ERβ pathway deficiency might enhance GEN–CIS bioactivity via the downregulation of P53. In summary, our data imply that daily intake of GEN-rich diet could collaborate with CIS anti-tumor treatment in ERα−/ERβ− breast cancer cases. ERβ pathway might be one of the potential targets which elicit GEN’s positive effects in ERα− breast cancer patients. |
| abstract_unstemmed |
Abstract As one of the typical food-derived phytoestrogens, genistein (GEN) could bind to estrogen receptor (ER) and was reported to be closely related to breast cancer. Our former research showed that GEN interfered with the anti-tumor effects of cisplatin (CIS) in breast cancer MCF-7 (ERα+/ERβ−) cells. However, it is not clear whether ER expression pattern affects GEN’s modulation on CIS’s activity. In the present study, breast cancer ERβ knockdown (ERβKD) MDA-MB-231 (ERα−/ERβ+) cell model was established via ERβ RNAi lentivirus infection. The role of ERβ expression in GEN’s bioeffects on cells’ response to CIS was investigated and was further double-checked by pathway-specific inhibitor PHTPP. Consistent results were harvested through cell viability analysis, cell cycle distribution flow cytometry, TUNEL staining, and expression detection of key biomarkers, Bax, Bcl-2, P21, P53, and cleaved caspase-3. Compared with the control group, PHTPP-treated or ERβKD cells exhibited higher sensitivity to both GEN and CIS treatment. GEN and CIS showed synergistic effects only in ERβ-deficient cells. This effect mainly resulted in G2 phase arresting and apoptosis induction with the upregulation of P21 and Bax/Bcl-2 protein level. Besides, P53 expression was strikingly suppressed in ERβ-deficient cells. This indicated ERβ pathway deficiency might enhance GEN–CIS bioactivity via the downregulation of P53. In summary, our data imply that daily intake of GEN-rich diet could collaborate with CIS anti-tumor treatment in ERα−/ERβ− breast cancer cases. ERβ pathway might be one of the potential targets which elicit GEN’s positive effects in ERα− breast cancer patients. |
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ERβ modulates genistein’s cisplatin-enhancing activities in breast cancer MDA-MB-231 cells via P53-independent pathway |
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Our former research showed that GEN interfered with the anti-tumor effects of cisplatin (CIS) in breast cancer MCF-7 (ERα+/ERβ−) cells. However, it is not clear whether ER expression pattern affects GEN’s modulation on CIS’s activity. In the present study, breast cancer ERβ knockdown (ERβKD) MDA-MB-231 (ERα−/ERβ+) cell model was established via ERβ RNAi lentivirus infection. The role of ERβ expression in GEN’s bioeffects on cells’ response to CIS was investigated and was further double-checked by pathway-specific inhibitor PHTPP. Consistent results were harvested through cell viability analysis, cell cycle distribution flow cytometry, TUNEL staining, and expression detection of key biomarkers, Bax, Bcl-2, P21, P53, and cleaved caspase-3. Compared with the control group, PHTPP-treated or ERβKD cells exhibited higher sensitivity to both GEN and CIS treatment. GEN and CIS showed synergistic effects only in ERβ-deficient cells. 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