Caffeic acid phenethyl ester inhibits the growth of bladder carcinoma cells by upregulating growth differentiation factor 15

Background: Caffeic acid phenethyl ester (CAPE), a bioactive component of propolis, has beneficial effects on cancer prevention. Growth differentiation factor 15 (GDF15) is an antitumor gene of bladder cancer. Therefore, this study investigated the anti-cancer effect of CAPE on bladder carcinoma cel...
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Autor*in:	Chen-Pang Hou [verfasserIn] Ke-Hung Tsui [verfasserIn] Kang-Shuo Chang [verfasserIn] Hsin-Ching Sung [verfasserIn] Shu-Yuan Hsu [verfasserIn] Yu-Hsiang Lin [verfasserIn] Pei-Shan Yang [verfasserIn] Chien-Lun Chen [verfasserIn] Tsui-Hsia Feng [verfasserIn] Horng-Heng Juang [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2022

Schlagwörter:	Bladder GDF15 CAPE AMPK MAPK NDRG1

Übergeordnetes Werk:	In: Biomedical Journal - Elsevier, 2013, 45(2022), 5, Seite 763-775
Übergeordnetes Werk:	volume:45 ; year:2022 ; number:5 ; pages:763-775

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.1016/j.bj.2021.10.006

Katalog-ID:	DOAJ020848420

Internformat


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520			\|a Background: Caffeic acid phenethyl ester (CAPE), a bioactive component of propolis, has beneficial effects on cancer prevention. Growth differentiation factor 15 (GDF15) is an antitumor gene of bladder cancer. Therefore, this study investigated the anti-cancer effect of CAPE on bladder carcinoma cells and related mechanisms. Methods: The expressions of GDF15, N-myc downstream-regulated gene 1 (NDRG1), and maspin, and the activations of extracellular signal regulated kinase (ERK), c-jun Nterminal kinase (JNK), p38, and 50 adenosine monophosphate-activated protein kinase (AMPK) α1/2 in human bladder cells after gene transfection or knockdown were determined by immunoblot, real-time reverse transcriptase-polymerase chain reaction (RT-qPCR), and reporter assays. The assays of 5-ethynyl-2′-deoxyuridine (EdU), CyQUANT cell proliferation, and Matrigel invasion, and the xenograft animal study were used to assess the cell proliferation, invasion, and tumorigenesis. Results: GDF15 expression in epithelial cells was negatively correlated with neoplasia in vitro. Also, GDF15 exhibits in bladder fibroblasts and smooth muscle cells. CAPE-induced expressions of NDRG1 and maspin decreased cell proliferation and invasion of bladder carcinoma cells in a GDF15-dependent manner in vitro. The xenograft animal study suggesting CAPE attenuated tumor growth in vivo. CAPE increased phosphorylation of ERK, JNK, p38, and AMPKα1/2 to modulate the GDF15 expressions. Pretreatments with ERK, JNK, or p38 inhibitors partially inhibited the CAPE effects on the inductions of GDF15, NDRG1, or maspin. Knockdown of AMPKα1/2 attenuated the CAPE-induced GDF15 expression and cell proliferation in bladder carcinoma cells. Conclusions: Our findings indicate that CAPE is a promising agent for anti-tumor growth in human bladder carcinoma cells via the upregulation of GDF15.
650		4	\|a Bladder
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700	0		\|a Horng-Heng Juang \|e verfasserin \|4 aut
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allfields	10.1016/j.bj.2021.10.006 doi (DE-627)DOAJ020848420 (DE-599)DOAJc4661ed6681848b5949bbd33b188e841 DE-627 ger DE-627 rakwb eng R5-920 QH301-705.5 Chen-Pang Hou verfasserin aut Caffeic acid phenethyl ester inhibits the growth of bladder carcinoma cells by upregulating growth differentiation factor 15 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background: Caffeic acid phenethyl ester (CAPE), a bioactive component of propolis, has beneficial effects on cancer prevention. Growth differentiation factor 15 (GDF15) is an antitumor gene of bladder cancer. Therefore, this study investigated the anti-cancer effect of CAPE on bladder carcinoma cells and related mechanisms. Methods: The expressions of GDF15, N-myc downstream-regulated gene 1 (NDRG1), and maspin, and the activations of extracellular signal regulated kinase (ERK), c-jun Nterminal kinase (JNK), p38, and 50 adenosine monophosphate-activated protein kinase (AMPK) α1/2 in human bladder cells after gene transfection or knockdown were determined by immunoblot, real-time reverse transcriptase-polymerase chain reaction (RT-qPCR), and reporter assays. The assays of 5-ethynyl-2′-deoxyuridine (EdU), CyQUANT cell proliferation, and Matrigel invasion, and the xenograft animal study were used to assess the cell proliferation, invasion, and tumorigenesis. Results: GDF15 expression in epithelial cells was negatively correlated with neoplasia in vitro. Also, GDF15 exhibits in bladder fibroblasts and smooth muscle cells. CAPE-induced expressions of NDRG1 and maspin decreased cell proliferation and invasion of bladder carcinoma cells in a GDF15-dependent manner in vitro. The xenograft animal study suggesting CAPE attenuated tumor growth in vivo. CAPE increased phosphorylation of ERK, JNK, p38, and AMPKα1/2 to modulate the GDF15 expressions. Pretreatments with ERK, JNK, or p38 inhibitors partially inhibited the CAPE effects on the inductions of GDF15, NDRG1, or maspin. Knockdown of AMPKα1/2 attenuated the CAPE-induced GDF15 expression and cell proliferation in bladder carcinoma cells. Conclusions: Our findings indicate that CAPE is a promising agent for anti-tumor growth in human bladder carcinoma cells via the upregulation of GDF15. Bladder GDF15 CAPE AMPK MAPK NDRG1 Medicine (General) Biology (General) Ke-Hung Tsui verfasserin aut Kang-Shuo Chang verfasserin aut Hsin-Ching Sung verfasserin aut Shu-Yuan Hsu verfasserin aut Yu-Hsiang Lin verfasserin aut Pei-Shan Yang verfasserin aut Chien-Lun Chen verfasserin aut Tsui-Hsia Feng verfasserin aut Horng-Heng Juang verfasserin aut In Biomedical Journal Elsevier, 2013 45(2022), 5, Seite 763-775 (DE-627)734738153 (DE-600)2698541-X 23202890 nnns volume:45 year:2022 number:5 pages:763-775 https://doi.org/10.1016/j.bj.2021.10.006 kostenfrei https://doaj.org/article/c4661ed6681848b5949bbd33b188e841 kostenfrei http://www.sciencedirect.com/science/article/pii/S2319417021001414 kostenfrei https://doaj.org/toc/2319-4170 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 45 2022 5 763-775
spelling	10.1016/j.bj.2021.10.006 doi (DE-627)DOAJ020848420 (DE-599)DOAJc4661ed6681848b5949bbd33b188e841 DE-627 ger DE-627 rakwb eng R5-920 QH301-705.5 Chen-Pang Hou verfasserin aut Caffeic acid phenethyl ester inhibits the growth of bladder carcinoma cells by upregulating growth differentiation factor 15 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background: Caffeic acid phenethyl ester (CAPE), a bioactive component of propolis, has beneficial effects on cancer prevention. Growth differentiation factor 15 (GDF15) is an antitumor gene of bladder cancer. Therefore, this study investigated the anti-cancer effect of CAPE on bladder carcinoma cells and related mechanisms. Methods: The expressions of GDF15, N-myc downstream-regulated gene 1 (NDRG1), and maspin, and the activations of extracellular signal regulated kinase (ERK), c-jun Nterminal kinase (JNK), p38, and 50 adenosine monophosphate-activated protein kinase (AMPK) α1/2 in human bladder cells after gene transfection or knockdown were determined by immunoblot, real-time reverse transcriptase-polymerase chain reaction (RT-qPCR), and reporter assays. The assays of 5-ethynyl-2′-deoxyuridine (EdU), CyQUANT cell proliferation, and Matrigel invasion, and the xenograft animal study were used to assess the cell proliferation, invasion, and tumorigenesis. Results: GDF15 expression in epithelial cells was negatively correlated with neoplasia in vitro. Also, GDF15 exhibits in bladder fibroblasts and smooth muscle cells. CAPE-induced expressions of NDRG1 and maspin decreased cell proliferation and invasion of bladder carcinoma cells in a GDF15-dependent manner in vitro. The xenograft animal study suggesting CAPE attenuated tumor growth in vivo. CAPE increased phosphorylation of ERK, JNK, p38, and AMPKα1/2 to modulate the GDF15 expressions. Pretreatments with ERK, JNK, or p38 inhibitors partially inhibited the CAPE effects on the inductions of GDF15, NDRG1, or maspin. Knockdown of AMPKα1/2 attenuated the CAPE-induced GDF15 expression and cell proliferation in bladder carcinoma cells. Conclusions: Our findings indicate that CAPE is a promising agent for anti-tumor growth in human bladder carcinoma cells via the upregulation of GDF15. Bladder GDF15 CAPE AMPK MAPK NDRG1 Medicine (General) Biology (General) Ke-Hung Tsui verfasserin aut Kang-Shuo Chang verfasserin aut Hsin-Ching Sung verfasserin aut Shu-Yuan Hsu verfasserin aut Yu-Hsiang Lin verfasserin aut Pei-Shan Yang verfasserin aut Chien-Lun Chen verfasserin aut Tsui-Hsia Feng verfasserin aut Horng-Heng Juang verfasserin aut In Biomedical Journal Elsevier, 2013 45(2022), 5, Seite 763-775 (DE-627)734738153 (DE-600)2698541-X 23202890 nnns volume:45 year:2022 number:5 pages:763-775 https://doi.org/10.1016/j.bj.2021.10.006 kostenfrei https://doaj.org/article/c4661ed6681848b5949bbd33b188e841 kostenfrei http://www.sciencedirect.com/science/article/pii/S2319417021001414 kostenfrei https://doaj.org/toc/2319-4170 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 45 2022 5 763-775
allfields_unstemmed	10.1016/j.bj.2021.10.006 doi (DE-627)DOAJ020848420 (DE-599)DOAJc4661ed6681848b5949bbd33b188e841 DE-627 ger DE-627 rakwb eng R5-920 QH301-705.5 Chen-Pang Hou verfasserin aut Caffeic acid phenethyl ester inhibits the growth of bladder carcinoma cells by upregulating growth differentiation factor 15 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background: Caffeic acid phenethyl ester (CAPE), a bioactive component of propolis, has beneficial effects on cancer prevention. Growth differentiation factor 15 (GDF15) is an antitumor gene of bladder cancer. Therefore, this study investigated the anti-cancer effect of CAPE on bladder carcinoma cells and related mechanisms. Methods: The expressions of GDF15, N-myc downstream-regulated gene 1 (NDRG1), and maspin, and the activations of extracellular signal regulated kinase (ERK), c-jun Nterminal kinase (JNK), p38, and 50 adenosine monophosphate-activated protein kinase (AMPK) α1/2 in human bladder cells after gene transfection or knockdown were determined by immunoblot, real-time reverse transcriptase-polymerase chain reaction (RT-qPCR), and reporter assays. The assays of 5-ethynyl-2′-deoxyuridine (EdU), CyQUANT cell proliferation, and Matrigel invasion, and the xenograft animal study were used to assess the cell proliferation, invasion, and tumorigenesis. Results: GDF15 expression in epithelial cells was negatively correlated with neoplasia in vitro. Also, GDF15 exhibits in bladder fibroblasts and smooth muscle cells. CAPE-induced expressions of NDRG1 and maspin decreased cell proliferation and invasion of bladder carcinoma cells in a GDF15-dependent manner in vitro. The xenograft animal study suggesting CAPE attenuated tumor growth in vivo. CAPE increased phosphorylation of ERK, JNK, p38, and AMPKα1/2 to modulate the GDF15 expressions. Pretreatments with ERK, JNK, or p38 inhibitors partially inhibited the CAPE effects on the inductions of GDF15, NDRG1, or maspin. Knockdown of AMPKα1/2 attenuated the CAPE-induced GDF15 expression and cell proliferation in bladder carcinoma cells. Conclusions: Our findings indicate that CAPE is a promising agent for anti-tumor growth in human bladder carcinoma cells via the upregulation of GDF15. Bladder GDF15 CAPE AMPK MAPK NDRG1 Medicine (General) Biology (General) Ke-Hung Tsui verfasserin aut Kang-Shuo Chang verfasserin aut Hsin-Ching Sung verfasserin aut Shu-Yuan Hsu verfasserin aut Yu-Hsiang Lin verfasserin aut Pei-Shan Yang verfasserin aut Chien-Lun Chen verfasserin aut Tsui-Hsia Feng verfasserin aut Horng-Heng Juang verfasserin aut In Biomedical Journal Elsevier, 2013 45(2022), 5, Seite 763-775 (DE-627)734738153 (DE-600)2698541-X 23202890 nnns volume:45 year:2022 number:5 pages:763-775 https://doi.org/10.1016/j.bj.2021.10.006 kostenfrei https://doaj.org/article/c4661ed6681848b5949bbd33b188e841 kostenfrei http://www.sciencedirect.com/science/article/pii/S2319417021001414 kostenfrei https://doaj.org/toc/2319-4170 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 45 2022 5 763-775
allfieldsGer	10.1016/j.bj.2021.10.006 doi (DE-627)DOAJ020848420 (DE-599)DOAJc4661ed6681848b5949bbd33b188e841 DE-627 ger DE-627 rakwb eng R5-920 QH301-705.5 Chen-Pang Hou verfasserin aut Caffeic acid phenethyl ester inhibits the growth of bladder carcinoma cells by upregulating growth differentiation factor 15 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background: Caffeic acid phenethyl ester (CAPE), a bioactive component of propolis, has beneficial effects on cancer prevention. Growth differentiation factor 15 (GDF15) is an antitumor gene of bladder cancer. Therefore, this study investigated the anti-cancer effect of CAPE on bladder carcinoma cells and related mechanisms. Methods: The expressions of GDF15, N-myc downstream-regulated gene 1 (NDRG1), and maspin, and the activations of extracellular signal regulated kinase (ERK), c-jun Nterminal kinase (JNK), p38, and 50 adenosine monophosphate-activated protein kinase (AMPK) α1/2 in human bladder cells after gene transfection or knockdown were determined by immunoblot, real-time reverse transcriptase-polymerase chain reaction (RT-qPCR), and reporter assays. The assays of 5-ethynyl-2′-deoxyuridine (EdU), CyQUANT cell proliferation, and Matrigel invasion, and the xenograft animal study were used to assess the cell proliferation, invasion, and tumorigenesis. Results: GDF15 expression in epithelial cells was negatively correlated with neoplasia in vitro. Also, GDF15 exhibits in bladder fibroblasts and smooth muscle cells. CAPE-induced expressions of NDRG1 and maspin decreased cell proliferation and invasion of bladder carcinoma cells in a GDF15-dependent manner in vitro. The xenograft animal study suggesting CAPE attenuated tumor growth in vivo. CAPE increased phosphorylation of ERK, JNK, p38, and AMPKα1/2 to modulate the GDF15 expressions. Pretreatments with ERK, JNK, or p38 inhibitors partially inhibited the CAPE effects on the inductions of GDF15, NDRG1, or maspin. Knockdown of AMPKα1/2 attenuated the CAPE-induced GDF15 expression and cell proliferation in bladder carcinoma cells. Conclusions: Our findings indicate that CAPE is a promising agent for anti-tumor growth in human bladder carcinoma cells via the upregulation of GDF15. Bladder GDF15 CAPE AMPK MAPK NDRG1 Medicine (General) Biology (General) Ke-Hung Tsui verfasserin aut Kang-Shuo Chang verfasserin aut Hsin-Ching Sung verfasserin aut Shu-Yuan Hsu verfasserin aut Yu-Hsiang Lin verfasserin aut Pei-Shan Yang verfasserin aut Chien-Lun Chen verfasserin aut Tsui-Hsia Feng verfasserin aut Horng-Heng Juang verfasserin aut In Biomedical Journal Elsevier, 2013 45(2022), 5, Seite 763-775 (DE-627)734738153 (DE-600)2698541-X 23202890 nnns volume:45 year:2022 number:5 pages:763-775 https://doi.org/10.1016/j.bj.2021.10.006 kostenfrei https://doaj.org/article/c4661ed6681848b5949bbd33b188e841 kostenfrei http://www.sciencedirect.com/science/article/pii/S2319417021001414 kostenfrei https://doaj.org/toc/2319-4170 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 45 2022 5 763-775
allfieldsSound	10.1016/j.bj.2021.10.006 doi (DE-627)DOAJ020848420 (DE-599)DOAJc4661ed6681848b5949bbd33b188e841 DE-627 ger DE-627 rakwb eng R5-920 QH301-705.5 Chen-Pang Hou verfasserin aut Caffeic acid phenethyl ester inhibits the growth of bladder carcinoma cells by upregulating growth differentiation factor 15 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background: Caffeic acid phenethyl ester (CAPE), a bioactive component of propolis, has beneficial effects on cancer prevention. Growth differentiation factor 15 (GDF15) is an antitumor gene of bladder cancer. Therefore, this study investigated the anti-cancer effect of CAPE on bladder carcinoma cells and related mechanisms. Methods: The expressions of GDF15, N-myc downstream-regulated gene 1 (NDRG1), and maspin, and the activations of extracellular signal regulated kinase (ERK), c-jun Nterminal kinase (JNK), p38, and 50 adenosine monophosphate-activated protein kinase (AMPK) α1/2 in human bladder cells after gene transfection or knockdown were determined by immunoblot, real-time reverse transcriptase-polymerase chain reaction (RT-qPCR), and reporter assays. The assays of 5-ethynyl-2′-deoxyuridine (EdU), CyQUANT cell proliferation, and Matrigel invasion, and the xenograft animal study were used to assess the cell proliferation, invasion, and tumorigenesis. Results: GDF15 expression in epithelial cells was negatively correlated with neoplasia in vitro. Also, GDF15 exhibits in bladder fibroblasts and smooth muscle cells. CAPE-induced expressions of NDRG1 and maspin decreased cell proliferation and invasion of bladder carcinoma cells in a GDF15-dependent manner in vitro. The xenograft animal study suggesting CAPE attenuated tumor growth in vivo. CAPE increased phosphorylation of ERK, JNK, p38, and AMPKα1/2 to modulate the GDF15 expressions. Pretreatments with ERK, JNK, or p38 inhibitors partially inhibited the CAPE effects on the inductions of GDF15, NDRG1, or maspin. Knockdown of AMPKα1/2 attenuated the CAPE-induced GDF15 expression and cell proliferation in bladder carcinoma cells. Conclusions: Our findings indicate that CAPE is a promising agent for anti-tumor growth in human bladder carcinoma cells via the upregulation of GDF15. Bladder GDF15 CAPE AMPK MAPK NDRG1 Medicine (General) Biology (General) Ke-Hung Tsui verfasserin aut Kang-Shuo Chang verfasserin aut Hsin-Ching Sung verfasserin aut Shu-Yuan Hsu verfasserin aut Yu-Hsiang Lin verfasserin aut Pei-Shan Yang verfasserin aut Chien-Lun Chen verfasserin aut Tsui-Hsia Feng verfasserin aut Horng-Heng Juang verfasserin aut In Biomedical Journal Elsevier, 2013 45(2022), 5, Seite 763-775 (DE-627)734738153 (DE-600)2698541-X 23202890 nnns volume:45 year:2022 number:5 pages:763-775 https://doi.org/10.1016/j.bj.2021.10.006 kostenfrei https://doaj.org/article/c4661ed6681848b5949bbd33b188e841 kostenfrei http://www.sciencedirect.com/science/article/pii/S2319417021001414 kostenfrei https://doaj.org/toc/2319-4170 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 45 2022 5 763-775
language	English
source	In Biomedical Journal 45(2022), 5, Seite 763-775 volume:45 year:2022 number:5 pages:763-775
sourceStr	In Biomedical Journal 45(2022), 5, Seite 763-775 volume:45 year:2022 number:5 pages:763-775
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Bladder GDF15 CAPE AMPK MAPK NDRG1 Medicine (General) Biology (General)
isfreeaccess_bool	true
container_title	Biomedical Journal
authorswithroles_txt_mv	Chen-Pang Hou @@aut@@ Ke-Hung Tsui @@aut@@ Kang-Shuo Chang @@aut@@ Hsin-Ching Sung @@aut@@ Shu-Yuan Hsu @@aut@@ Yu-Hsiang Lin @@aut@@ Pei-Shan Yang @@aut@@ Chien-Lun Chen @@aut@@ Tsui-Hsia Feng @@aut@@ Horng-Heng Juang @@aut@@
publishDateDaySort_date	2022-01-01T00:00:00Z
hierarchy_top_id	734738153
id	DOAJ020848420
language_de	englisch
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Also, GDF15 exhibits in bladder fibroblasts and smooth muscle cells. CAPE-induced expressions of NDRG1 and maspin decreased cell proliferation and invasion of bladder carcinoma cells in a GDF15-dependent manner in vitro. The xenograft animal study suggesting CAPE attenuated tumor growth in vivo. CAPE increased phosphorylation of ERK, JNK, p38, and AMPKα1/2 to modulate the GDF15 expressions. Pretreatments with ERK, JNK, or p38 inhibitors partially inhibited the CAPE effects on the inductions of GDF15, NDRG1, or maspin. Knockdown of AMPKα1/2 attenuated the CAPE-induced GDF15 expression and cell proliferation in bladder carcinoma cells. 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callnumber-first	R - Medicine
author	Chen-Pang Hou
spellingShingle	Chen-Pang Hou misc R5-920 misc QH301-705.5 misc Bladder misc GDF15 misc CAPE misc AMPK misc MAPK misc NDRG1 misc Medicine (General) misc Biology (General) Caffeic acid phenethyl ester inhibits the growth of bladder carcinoma cells by upregulating growth differentiation factor 15
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topic_title	R5-920 QH301-705.5 Caffeic acid phenethyl ester inhibits the growth of bladder carcinoma cells by upregulating growth differentiation factor 15 Bladder GDF15 CAPE AMPK MAPK NDRG1
topic	misc R5-920 misc QH301-705.5 misc Bladder misc GDF15 misc CAPE misc AMPK misc MAPK misc NDRG1 misc Medicine (General) misc Biology (General)
topic_unstemmed	misc R5-920 misc QH301-705.5 misc Bladder misc GDF15 misc CAPE misc AMPK misc MAPK misc NDRG1 misc Medicine (General) misc Biology (General)
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title	Caffeic acid phenethyl ester inhibits the growth of bladder carcinoma cells by upregulating growth differentiation factor 15
ctrlnum	(DE-627)DOAJ020848420 (DE-599)DOAJc4661ed6681848b5949bbd33b188e841
title_full	Caffeic acid phenethyl ester inhibits the growth of bladder carcinoma cells by upregulating growth differentiation factor 15
author_sort	Chen-Pang Hou
journal	Biomedical Journal
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author_browse	Chen-Pang Hou Ke-Hung Tsui Kang-Shuo Chang Hsin-Ching Sung Shu-Yuan Hsu Yu-Hsiang Lin Pei-Shan Yang Chien-Lun Chen Tsui-Hsia Feng Horng-Heng Juang
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author-letter	Chen-Pang Hou
doi_str_mv	10.1016/j.bj.2021.10.006
author2-role	verfasserin
title_sort	caffeic acid phenethyl ester inhibits the growth of bladder carcinoma cells by upregulating growth differentiation factor 15
callnumber	R5-920
title_auth	Caffeic acid phenethyl ester inhibits the growth of bladder carcinoma cells by upregulating growth differentiation factor 15
abstract	Background: Caffeic acid phenethyl ester (CAPE), a bioactive component of propolis, has beneficial effects on cancer prevention. Growth differentiation factor 15 (GDF15) is an antitumor gene of bladder cancer. Therefore, this study investigated the anti-cancer effect of CAPE on bladder carcinoma cells and related mechanisms. Methods: The expressions of GDF15, N-myc downstream-regulated gene 1 (NDRG1), and maspin, and the activations of extracellular signal regulated kinase (ERK), c-jun Nterminal kinase (JNK), p38, and 50 adenosine monophosphate-activated protein kinase (AMPK) α1/2 in human bladder cells after gene transfection or knockdown were determined by immunoblot, real-time reverse transcriptase-polymerase chain reaction (RT-qPCR), and reporter assays. The assays of 5-ethynyl-2′-deoxyuridine (EdU), CyQUANT cell proliferation, and Matrigel invasion, and the xenograft animal study were used to assess the cell proliferation, invasion, and tumorigenesis. Results: GDF15 expression in epithelial cells was negatively correlated with neoplasia in vitro. Also, GDF15 exhibits in bladder fibroblasts and smooth muscle cells. CAPE-induced expressions of NDRG1 and maspin decreased cell proliferation and invasion of bladder carcinoma cells in a GDF15-dependent manner in vitro. The xenograft animal study suggesting CAPE attenuated tumor growth in vivo. CAPE increased phosphorylation of ERK, JNK, p38, and AMPKα1/2 to modulate the GDF15 expressions. Pretreatments with ERK, JNK, or p38 inhibitors partially inhibited the CAPE effects on the inductions of GDF15, NDRG1, or maspin. Knockdown of AMPKα1/2 attenuated the CAPE-induced GDF15 expression and cell proliferation in bladder carcinoma cells. Conclusions: Our findings indicate that CAPE is a promising agent for anti-tumor growth in human bladder carcinoma cells via the upregulation of GDF15.
abstractGer	Background: Caffeic acid phenethyl ester (CAPE), a bioactive component of propolis, has beneficial effects on cancer prevention. Growth differentiation factor 15 (GDF15) is an antitumor gene of bladder cancer. Therefore, this study investigated the anti-cancer effect of CAPE on bladder carcinoma cells and related mechanisms. Methods: The expressions of GDF15, N-myc downstream-regulated gene 1 (NDRG1), and maspin, and the activations of extracellular signal regulated kinase (ERK), c-jun Nterminal kinase (JNK), p38, and 50 adenosine monophosphate-activated protein kinase (AMPK) α1/2 in human bladder cells after gene transfection or knockdown were determined by immunoblot, real-time reverse transcriptase-polymerase chain reaction (RT-qPCR), and reporter assays. The assays of 5-ethynyl-2′-deoxyuridine (EdU), CyQUANT cell proliferation, and Matrigel invasion, and the xenograft animal study were used to assess the cell proliferation, invasion, and tumorigenesis. Results: GDF15 expression in epithelial cells was negatively correlated with neoplasia in vitro. Also, GDF15 exhibits in bladder fibroblasts and smooth muscle cells. CAPE-induced expressions of NDRG1 and maspin decreased cell proliferation and invasion of bladder carcinoma cells in a GDF15-dependent manner in vitro. The xenograft animal study suggesting CAPE attenuated tumor growth in vivo. CAPE increased phosphorylation of ERK, JNK, p38, and AMPKα1/2 to modulate the GDF15 expressions. Pretreatments with ERK, JNK, or p38 inhibitors partially inhibited the CAPE effects on the inductions of GDF15, NDRG1, or maspin. Knockdown of AMPKα1/2 attenuated the CAPE-induced GDF15 expression and cell proliferation in bladder carcinoma cells. Conclusions: Our findings indicate that CAPE is a promising agent for anti-tumor growth in human bladder carcinoma cells via the upregulation of GDF15.
abstract_unstemmed	Background: Caffeic acid phenethyl ester (CAPE), a bioactive component of propolis, has beneficial effects on cancer prevention. Growth differentiation factor 15 (GDF15) is an antitumor gene of bladder cancer. Therefore, this study investigated the anti-cancer effect of CAPE on bladder carcinoma cells and related mechanisms. Methods: The expressions of GDF15, N-myc downstream-regulated gene 1 (NDRG1), and maspin, and the activations of extracellular signal regulated kinase (ERK), c-jun Nterminal kinase (JNK), p38, and 50 adenosine monophosphate-activated protein kinase (AMPK) α1/2 in human bladder cells after gene transfection or knockdown were determined by immunoblot, real-time reverse transcriptase-polymerase chain reaction (RT-qPCR), and reporter assays. The assays of 5-ethynyl-2′-deoxyuridine (EdU), CyQUANT cell proliferation, and Matrigel invasion, and the xenograft animal study were used to assess the cell proliferation, invasion, and tumorigenesis. Results: GDF15 expression in epithelial cells was negatively correlated with neoplasia in vitro. Also, GDF15 exhibits in bladder fibroblasts and smooth muscle cells. CAPE-induced expressions of NDRG1 and maspin decreased cell proliferation and invasion of bladder carcinoma cells in a GDF15-dependent manner in vitro. The xenograft animal study suggesting CAPE attenuated tumor growth in vivo. CAPE increased phosphorylation of ERK, JNK, p38, and AMPKα1/2 to modulate the GDF15 expressions. Pretreatments with ERK, JNK, or p38 inhibitors partially inhibited the CAPE effects on the inductions of GDF15, NDRG1, or maspin. Knockdown of AMPKα1/2 attenuated the CAPE-induced GDF15 expression and cell proliferation in bladder carcinoma cells. Conclusions: Our findings indicate that CAPE is a promising agent for anti-tumor growth in human bladder carcinoma cells via the upregulation of GDF15.
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title_short	Caffeic acid phenethyl ester inhibits the growth of bladder carcinoma cells by upregulating growth differentiation factor 15
url	https://doi.org/10.1016/j.bj.2021.10.006 https://doaj.org/article/c4661ed6681848b5949bbd33b188e841 http://www.sciencedirect.com/science/article/pii/S2319417021001414 https://doaj.org/toc/2319-4170
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author2	Ke-Hung Tsui Kang-Shuo Chang Hsin-Ching Sung Shu-Yuan Hsu Yu-Hsiang Lin Pei-Shan Yang Chien-Lun Chen Tsui-Hsia Feng Horng-Heng Juang
author2Str	Ke-Hung Tsui Kang-Shuo Chang Hsin-Ching Sung Shu-Yuan Hsu Yu-Hsiang Lin Pei-Shan Yang Chien-Lun Chen Tsui-Hsia Feng Horng-Heng Juang
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doi_str	10.1016/j.bj.2021.10.006
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up_date	2024-07-03T17:22:06.612Z
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