Pioglitazone, an agonist of PPARγ, reverses doxorubicin-resistance in an osteosarcoma patient-derived orthotopic xenograft model by downregulating P-glycoprotein expression

Multidrug resistance (MDR) which results in chemoresistance is a major problem in osteosarcoma. P-glycoprotein (P-gp) plays a critical role in MDR by pumping out chemotherapy agents. Peroxisome proliferator activated receptor gamma (PPARγ) is a nuclear receptor involved in cellular differentiation a...
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Gespeichert in:

Autor*in:	Higuchi, Takashi [verfasserIn] Sugisawa, Norihiko [verfasserIn] Miyake, Kentaro [verfasserIn] Oshiro, Hiromichi [verfasserIn] Yamamoto, Norio [verfasserIn] Hayashi, Katsuhiro [verfasserIn] Kimura, Hiroaki [verfasserIn] Miwa, Shinji [verfasserIn] Igarashi, Kentaro [verfasserIn] Kline, Zoey [verfasserIn] Bouvet, Michael [verfasserIn] Singh, Shree Ram [verfasserIn] Tsuchiya, Hiroyuki [verfasserIn] Hoffman, Robert M. [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2019

Schlagwörter:	Osteosarcoma Pioglitazone Doxorubicin Drug resistancy Patient-derived Orthotopic xenograft PDOX PPARγ

Übergeordnetes Werk:	Enthalten in: Biomedicine & pharmacotherapy - Amsterdam [u.a.] : Elsevier Science, 1989, 118
Übergeordnetes Werk:	volume:118

DOI / URN:	10.1016/j.biopha.2019.109356

Katalog-ID:	ELV002887592

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245	1	0	\|a Pioglitazone, an agonist of PPARγ, reverses doxorubicin-resistance in an osteosarcoma patient-derived orthotopic xenograft model by downregulating P-glycoprotein expression
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520			\|a Multidrug resistance (MDR) which results in chemoresistance is a major problem in osteosarcoma. P-glycoprotein (P-gp) plays a critical role in MDR by pumping out chemotherapy agents. Peroxisome proliferator activated receptor gamma (PPARγ) is a nuclear receptor involved in cellular differentiation and proliferation. Recently, a correlation between the expression and activity of PPARγ and the expression of P-gp-associated with MDR, has been reported in several human cancers. The present study determined if pioglitazone (PIO), a PPARγ agonist, could modulate P-gp and overcome doxorubicin (DOX)-resistance in a patient-derived orthotopic xenograft (PDOX) model of osteosarcoma. P-gp mRNA expression was quantified in 143B human osteosarcoma cells treated with DOX with/without PIO. The osteosarcoma PDOX models were randomized into four treatment groups of six mice: Control; PIO alone; DOX alone; DOX and PIO combination. Tumor size and body weight were measured during the 14 days of treatment. DOX significantly induced P-gp mRNA in a dose-dependent manner in 143B cells. PIO inhibited the increase of P-gp mRNA induced by DOX treatment when co-administrated with DOX. Tumor growth was inhibited the most by the DOX-PIO combination. Tumors treated with the DOX-PIO combination also had the most tumor necrosis. This study suggests that the DOX-PIO combination could be used in the clinic for osteosarcoma patients who develop DOX-resistance.
650		4	\|a Osteosarcoma
650		4	\|a Pioglitazone
650		4	\|a Doxorubicin
650		4	\|a Drug resistancy
650		4	\|a Patient-derived
650		4	\|a Orthotopic xenograft
650		4	\|a PDOX
650		4	\|a PPARγ
700	1		\|a Sugisawa, Norihiko \|e verfasserin \|4 aut
700	1		\|a Miyake, Kentaro \|e verfasserin \|4 aut
700	1		\|a Oshiro, Hiromichi \|e verfasserin \|4 aut
700	1		\|a Yamamoto, Norio \|e verfasserin \|4 aut
700	1		\|a Hayashi, Katsuhiro \|e verfasserin \|4 aut
700	1		\|a Kimura, Hiroaki \|e verfasserin \|4 aut
700	1		\|a Miwa, Shinji \|e verfasserin \|4 aut
700	1		\|a Igarashi, Kentaro \|e verfasserin \|4 aut
700	1		\|a Kline, Zoey \|e verfasserin \|4 aut
700	1		\|a Bouvet, Michael \|e verfasserin \|4 aut
700	1		\|a Singh, Shree Ram \|e verfasserin \|4 aut
700	1		\|a Tsuchiya, Hiroyuki \|e verfasserin \|4 aut
700	1		\|a Hoffman, Robert M. \|e verfasserin \|4 aut
773	0	8	\|i Enthalten in \|t Biomedicine & pharmacotherapy \|d Amsterdam [u.a.] : Elsevier Science, 1989 \|g 118 \|h Online-Ressource \|w (DE-627)306717565 \|w (DE-600)1501510-5 \|w (DE-576)261593021 \|x 1950-6007 \|7 nnns
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936	b	k	\|a 44.40 \|j Pharmazie \|j Pharmazeutika
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author_variant	t h th n s ns k m km h o ho n y ny k h kh h k hk s m sm k i ki z k zk m b mb s r s sr srs h t ht r m h rm rmh
matchkey_str	article:19506007:2019----::igiaoengnsoparvredxrbcneitnennsesroaaindrvdrhtpceorfmdl
hierarchy_sort_str	2019
bklnumber	44.40
publishDate	2019
allfields	10.1016/j.biopha.2019.109356 doi (DE-627)ELV002887592 (ELSEVIER)S0753-3322(19)33594-2 DE-627 ger DE-627 rda eng 610 DE-600 44.40 bkl Higuchi, Takashi verfasserin aut Pioglitazone, an agonist of PPARγ, reverses doxorubicin-resistance in an osteosarcoma patient-derived orthotopic xenograft model by downregulating P-glycoprotein expression 2019 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Multidrug resistance (MDR) which results in chemoresistance is a major problem in osteosarcoma. P-glycoprotein (P-gp) plays a critical role in MDR by pumping out chemotherapy agents. Peroxisome proliferator activated receptor gamma (PPARγ) is a nuclear receptor involved in cellular differentiation and proliferation. Recently, a correlation between the expression and activity of PPARγ and the expression of P-gp-associated with MDR, has been reported in several human cancers. The present study determined if pioglitazone (PIO), a PPARγ agonist, could modulate P-gp and overcome doxorubicin (DOX)-resistance in a patient-derived orthotopic xenograft (PDOX) model of osteosarcoma. P-gp mRNA expression was quantified in 143B human osteosarcoma cells treated with DOX with/without PIO. The osteosarcoma PDOX models were randomized into four treatment groups of six mice: Control; PIO alone; DOX alone; DOX and PIO combination. Tumor size and body weight were measured during the 14 days of treatment. DOX significantly induced P-gp mRNA in a dose-dependent manner in 143B cells. PIO inhibited the increase of P-gp mRNA induced by DOX treatment when co-administrated with DOX. Tumor growth was inhibited the most by the DOX-PIO combination. Tumors treated with the DOX-PIO combination also had the most tumor necrosis. This study suggests that the DOX-PIO combination could be used in the clinic for osteosarcoma patients who develop DOX-resistance. Osteosarcoma Pioglitazone Doxorubicin Drug resistancy Patient-derived Orthotopic xenograft PDOX PPARγ Sugisawa, Norihiko verfasserin aut Miyake, Kentaro verfasserin aut Oshiro, Hiromichi verfasserin aut Yamamoto, Norio verfasserin aut Hayashi, Katsuhiro verfasserin aut Kimura, Hiroaki verfasserin aut Miwa, Shinji verfasserin aut Igarashi, Kentaro verfasserin aut Kline, Zoey verfasserin aut Bouvet, Michael verfasserin aut Singh, Shree Ram verfasserin aut Tsuchiya, Hiroyuki verfasserin aut Hoffman, Robert M. verfasserin aut Enthalten in Biomedicine & pharmacotherapy Amsterdam [u.a.] : Elsevier Science, 1989 118 Online-Ressource (DE-627)306717565 (DE-600)1501510-5 (DE-576)261593021 1950-6007 nnns volume:118 GBV_USEFLAG_U SYSFLAG_U GBV_ELV SSG-OLC-PHA SSG-OPC-PHA 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_165 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2008 GBV_ILN_2014 GBV_ILN_2025 GBV_ILN_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2064 GBV_ILN_2106 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 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_4338 GBV_ILN_4367 GBV_ILN_4700 44.40 Pharmazie Pharmazeutika AR 118
spelling	10.1016/j.biopha.2019.109356 doi (DE-627)ELV002887592 (ELSEVIER)S0753-3322(19)33594-2 DE-627 ger DE-627 rda eng 610 DE-600 44.40 bkl Higuchi, Takashi verfasserin aut Pioglitazone, an agonist of PPARγ, reverses doxorubicin-resistance in an osteosarcoma patient-derived orthotopic xenograft model by downregulating P-glycoprotein expression 2019 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Multidrug resistance (MDR) which results in chemoresistance is a major problem in osteosarcoma. P-glycoprotein (P-gp) plays a critical role in MDR by pumping out chemotherapy agents. Peroxisome proliferator activated receptor gamma (PPARγ) is a nuclear receptor involved in cellular differentiation and proliferation. Recently, a correlation between the expression and activity of PPARγ and the expression of P-gp-associated with MDR, has been reported in several human cancers. The present study determined if pioglitazone (PIO), a PPARγ agonist, could modulate P-gp and overcome doxorubicin (DOX)-resistance in a patient-derived orthotopic xenograft (PDOX) model of osteosarcoma. P-gp mRNA expression was quantified in 143B human osteosarcoma cells treated with DOX with/without PIO. The osteosarcoma PDOX models were randomized into four treatment groups of six mice: Control; PIO alone; DOX alone; DOX and PIO combination. Tumor size and body weight were measured during the 14 days of treatment. DOX significantly induced P-gp mRNA in a dose-dependent manner in 143B cells. PIO inhibited the increase of P-gp mRNA induced by DOX treatment when co-administrated with DOX. Tumor growth was inhibited the most by the DOX-PIO combination. Tumors treated with the DOX-PIO combination also had the most tumor necrosis. This study suggests that the DOX-PIO combination could be used in the clinic for osteosarcoma patients who develop DOX-resistance. Osteosarcoma Pioglitazone Doxorubicin Drug resistancy Patient-derived Orthotopic xenograft PDOX PPARγ Sugisawa, Norihiko verfasserin aut Miyake, Kentaro verfasserin aut Oshiro, Hiromichi verfasserin aut Yamamoto, Norio verfasserin aut Hayashi, Katsuhiro verfasserin aut Kimura, Hiroaki verfasserin aut Miwa, Shinji verfasserin aut Igarashi, Kentaro verfasserin aut Kline, Zoey verfasserin aut Bouvet, Michael verfasserin aut Singh, Shree Ram verfasserin aut Tsuchiya, Hiroyuki verfasserin aut Hoffman, Robert M. verfasserin aut Enthalten in Biomedicine & pharmacotherapy Amsterdam [u.a.] : Elsevier Science, 1989 118 Online-Ressource (DE-627)306717565 (DE-600)1501510-5 (DE-576)261593021 1950-6007 nnns volume:118 GBV_USEFLAG_U SYSFLAG_U GBV_ELV SSG-OLC-PHA SSG-OPC-PHA 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_165 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2008 GBV_ILN_2014 GBV_ILN_2025 GBV_ILN_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2064 GBV_ILN_2106 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 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_4338 GBV_ILN_4367 GBV_ILN_4700 44.40 Pharmazie Pharmazeutika AR 118
allfields_unstemmed	10.1016/j.biopha.2019.109356 doi (DE-627)ELV002887592 (ELSEVIER)S0753-3322(19)33594-2 DE-627 ger DE-627 rda eng 610 DE-600 44.40 bkl Higuchi, Takashi verfasserin aut Pioglitazone, an agonist of PPARγ, reverses doxorubicin-resistance in an osteosarcoma patient-derived orthotopic xenograft model by downregulating P-glycoprotein expression 2019 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Multidrug resistance (MDR) which results in chemoresistance is a major problem in osteosarcoma. P-glycoprotein (P-gp) plays a critical role in MDR by pumping out chemotherapy agents. Peroxisome proliferator activated receptor gamma (PPARγ) is a nuclear receptor involved in cellular differentiation and proliferation. Recently, a correlation between the expression and activity of PPARγ and the expression of P-gp-associated with MDR, has been reported in several human cancers. The present study determined if pioglitazone (PIO), a PPARγ agonist, could modulate P-gp and overcome doxorubicin (DOX)-resistance in a patient-derived orthotopic xenograft (PDOX) model of osteosarcoma. P-gp mRNA expression was quantified in 143B human osteosarcoma cells treated with DOX with/without PIO. The osteosarcoma PDOX models were randomized into four treatment groups of six mice: Control; PIO alone; DOX alone; DOX and PIO combination. Tumor size and body weight were measured during the 14 days of treatment. DOX significantly induced P-gp mRNA in a dose-dependent manner in 143B cells. PIO inhibited the increase of P-gp mRNA induced by DOX treatment when co-administrated with DOX. Tumor growth was inhibited the most by the DOX-PIO combination. Tumors treated with the DOX-PIO combination also had the most tumor necrosis. This study suggests that the DOX-PIO combination could be used in the clinic for osteosarcoma patients who develop DOX-resistance. Osteosarcoma Pioglitazone Doxorubicin Drug resistancy Patient-derived Orthotopic xenograft PDOX PPARγ Sugisawa, Norihiko verfasserin aut Miyake, Kentaro verfasserin aut Oshiro, Hiromichi verfasserin aut Yamamoto, Norio verfasserin aut Hayashi, Katsuhiro verfasserin aut Kimura, Hiroaki verfasserin aut Miwa, Shinji verfasserin aut Igarashi, Kentaro verfasserin aut Kline, Zoey verfasserin aut Bouvet, Michael verfasserin aut Singh, Shree Ram verfasserin aut Tsuchiya, Hiroyuki verfasserin aut Hoffman, Robert M. verfasserin aut Enthalten in Biomedicine & pharmacotherapy Amsterdam [u.a.] : Elsevier Science, 1989 118 Online-Ressource (DE-627)306717565 (DE-600)1501510-5 (DE-576)261593021 1950-6007 nnns volume:118 GBV_USEFLAG_U SYSFLAG_U GBV_ELV SSG-OLC-PHA SSG-OPC-PHA 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_165 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2008 GBV_ILN_2014 GBV_ILN_2025 GBV_ILN_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2064 GBV_ILN_2106 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 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_4338 GBV_ILN_4367 GBV_ILN_4700 44.40 Pharmazie Pharmazeutika AR 118
allfieldsGer	10.1016/j.biopha.2019.109356 doi (DE-627)ELV002887592 (ELSEVIER)S0753-3322(19)33594-2 DE-627 ger DE-627 rda eng 610 DE-600 44.40 bkl Higuchi, Takashi verfasserin aut Pioglitazone, an agonist of PPARγ, reverses doxorubicin-resistance in an osteosarcoma patient-derived orthotopic xenograft model by downregulating P-glycoprotein expression 2019 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Multidrug resistance (MDR) which results in chemoresistance is a major problem in osteosarcoma. P-glycoprotein (P-gp) plays a critical role in MDR by pumping out chemotherapy agents. Peroxisome proliferator activated receptor gamma (PPARγ) is a nuclear receptor involved in cellular differentiation and proliferation. Recently, a correlation between the expression and activity of PPARγ and the expression of P-gp-associated with MDR, has been reported in several human cancers. The present study determined if pioglitazone (PIO), a PPARγ agonist, could modulate P-gp and overcome doxorubicin (DOX)-resistance in a patient-derived orthotopic xenograft (PDOX) model of osteosarcoma. P-gp mRNA expression was quantified in 143B human osteosarcoma cells treated with DOX with/without PIO. The osteosarcoma PDOX models were randomized into four treatment groups of six mice: Control; PIO alone; DOX alone; DOX and PIO combination. Tumor size and body weight were measured during the 14 days of treatment. DOX significantly induced P-gp mRNA in a dose-dependent manner in 143B cells. PIO inhibited the increase of P-gp mRNA induced by DOX treatment when co-administrated with DOX. Tumor growth was inhibited the most by the DOX-PIO combination. Tumors treated with the DOX-PIO combination also had the most tumor necrosis. This study suggests that the DOX-PIO combination could be used in the clinic for osteosarcoma patients who develop DOX-resistance. Osteosarcoma Pioglitazone Doxorubicin Drug resistancy Patient-derived Orthotopic xenograft PDOX PPARγ Sugisawa, Norihiko verfasserin aut Miyake, Kentaro verfasserin aut Oshiro, Hiromichi verfasserin aut Yamamoto, Norio verfasserin aut Hayashi, Katsuhiro verfasserin aut Kimura, Hiroaki verfasserin aut Miwa, Shinji verfasserin aut Igarashi, Kentaro verfasserin aut Kline, Zoey verfasserin aut Bouvet, Michael verfasserin aut Singh, Shree Ram verfasserin aut Tsuchiya, Hiroyuki verfasserin aut Hoffman, Robert M. verfasserin aut Enthalten in Biomedicine & pharmacotherapy Amsterdam [u.a.] : Elsevier Science, 1989 118 Online-Ressource (DE-627)306717565 (DE-600)1501510-5 (DE-576)261593021 1950-6007 nnns volume:118 GBV_USEFLAG_U SYSFLAG_U GBV_ELV SSG-OLC-PHA SSG-OPC-PHA 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_165 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2008 GBV_ILN_2014 GBV_ILN_2025 GBV_ILN_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2064 GBV_ILN_2106 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 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_4338 GBV_ILN_4367 GBV_ILN_4700 44.40 Pharmazie Pharmazeutika AR 118
allfieldsSound	10.1016/j.biopha.2019.109356 doi (DE-627)ELV002887592 (ELSEVIER)S0753-3322(19)33594-2 DE-627 ger DE-627 rda eng 610 DE-600 44.40 bkl Higuchi, Takashi verfasserin aut Pioglitazone, an agonist of PPARγ, reverses doxorubicin-resistance in an osteosarcoma patient-derived orthotopic xenograft model by downregulating P-glycoprotein expression 2019 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Multidrug resistance (MDR) which results in chemoresistance is a major problem in osteosarcoma. P-glycoprotein (P-gp) plays a critical role in MDR by pumping out chemotherapy agents. Peroxisome proliferator activated receptor gamma (PPARγ) is a nuclear receptor involved in cellular differentiation and proliferation. Recently, a correlation between the expression and activity of PPARγ and the expression of P-gp-associated with MDR, has been reported in several human cancers. The present study determined if pioglitazone (PIO), a PPARγ agonist, could modulate P-gp and overcome doxorubicin (DOX)-resistance in a patient-derived orthotopic xenograft (PDOX) model of osteosarcoma. P-gp mRNA expression was quantified in 143B human osteosarcoma cells treated with DOX with/without PIO. The osteosarcoma PDOX models were randomized into four treatment groups of six mice: Control; PIO alone; DOX alone; DOX and PIO combination. Tumor size and body weight were measured during the 14 days of treatment. DOX significantly induced P-gp mRNA in a dose-dependent manner in 143B cells. PIO inhibited the increase of P-gp mRNA induced by DOX treatment when co-administrated with DOX. Tumor growth was inhibited the most by the DOX-PIO combination. Tumors treated with the DOX-PIO combination also had the most tumor necrosis. This study suggests that the DOX-PIO combination could be used in the clinic for osteosarcoma patients who develop DOX-resistance. Osteosarcoma Pioglitazone Doxorubicin Drug resistancy Patient-derived Orthotopic xenograft PDOX PPARγ Sugisawa, Norihiko verfasserin aut Miyake, Kentaro verfasserin aut Oshiro, Hiromichi verfasserin aut Yamamoto, Norio verfasserin aut Hayashi, Katsuhiro verfasserin aut Kimura, Hiroaki verfasserin aut Miwa, Shinji verfasserin aut Igarashi, Kentaro verfasserin aut Kline, Zoey verfasserin aut Bouvet, Michael verfasserin aut Singh, Shree Ram verfasserin aut Tsuchiya, Hiroyuki verfasserin aut Hoffman, Robert M. verfasserin aut Enthalten in Biomedicine & pharmacotherapy Amsterdam [u.a.] : Elsevier Science, 1989 118 Online-Ressource (DE-627)306717565 (DE-600)1501510-5 (DE-576)261593021 1950-6007 nnns volume:118 GBV_USEFLAG_U SYSFLAG_U GBV_ELV SSG-OLC-PHA SSG-OPC-PHA 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_165 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2008 GBV_ILN_2014 GBV_ILN_2025 GBV_ILN_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2064 GBV_ILN_2106 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2122 GBV_ILN_2143 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 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_4338 GBV_ILN_4367 GBV_ILN_4700 44.40 Pharmazie Pharmazeutika AR 118
language	English
source	Enthalten in Biomedicine & pharmacotherapy 118 volume:118
sourceStr	Enthalten in Biomedicine & pharmacotherapy 118 volume:118
format_phy_str_mv	Article
bklname	Pharmazie Pharmazeutika
institution	findex.gbv.de
topic_facet	Osteosarcoma Pioglitazone Doxorubicin Drug resistancy Patient-derived Orthotopic xenograft PDOX PPARγ
dewey-raw	610
isfreeaccess_bool	false
container_title	Biomedicine & pharmacotherapy
authorswithroles_txt_mv	Higuchi, Takashi @@aut@@ Sugisawa, Norihiko @@aut@@ Miyake, Kentaro @@aut@@ Oshiro, Hiromichi @@aut@@ Yamamoto, Norio @@aut@@ Hayashi, Katsuhiro @@aut@@ Kimura, Hiroaki @@aut@@ Miwa, Shinji @@aut@@ Igarashi, Kentaro @@aut@@ Kline, Zoey @@aut@@ Bouvet, Michael @@aut@@ Singh, Shree Ram @@aut@@ Tsuchiya, Hiroyuki @@aut@@ Hoffman, Robert M. @@aut@@
publishDateDaySort_date	2019-01-01T00:00:00Z
hierarchy_top_id	306717565
dewey-sort	3610
id	ELV002887592
language_de	englisch
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author	Higuchi, Takashi
spellingShingle	Higuchi, Takashi ddc 610 bkl 44.40 misc Osteosarcoma misc Pioglitazone misc Doxorubicin misc Drug resistancy misc Patient-derived misc Orthotopic xenograft misc PDOX misc PPARγ Pioglitazone, an agonist of PPARγ, reverses doxorubicin-resistance in an osteosarcoma patient-derived orthotopic xenograft model by downregulating P-glycoprotein expression
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topic_title	610 DE-600 44.40 bkl Pioglitazone, an agonist of PPARγ, reverses doxorubicin-resistance in an osteosarcoma patient-derived orthotopic xenograft model by downregulating P-glycoprotein expression Osteosarcoma Pioglitazone Doxorubicin Drug resistancy Patient-derived Orthotopic xenograft PDOX PPARγ
topic	ddc 610 bkl 44.40 misc Osteosarcoma misc Pioglitazone misc Doxorubicin misc Drug resistancy misc Patient-derived misc Orthotopic xenograft misc PDOX misc PPARγ
topic_unstemmed	ddc 610 bkl 44.40 misc Osteosarcoma misc Pioglitazone misc Doxorubicin misc Drug resistancy misc Patient-derived misc Orthotopic xenograft misc PDOX misc PPARγ
topic_browse	ddc 610 bkl 44.40 misc Osteosarcoma misc Pioglitazone misc Doxorubicin misc Drug resistancy misc Patient-derived misc Orthotopic xenograft misc PDOX misc PPARγ
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title	Pioglitazone, an agonist of PPARγ, reverses doxorubicin-resistance in an osteosarcoma patient-derived orthotopic xenograft model by downregulating P-glycoprotein expression
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title_full	Pioglitazone, an agonist of PPARγ, reverses doxorubicin-resistance in an osteosarcoma patient-derived orthotopic xenograft model by downregulating P-glycoprotein expression
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author_browse	Higuchi, Takashi Sugisawa, Norihiko Miyake, Kentaro Oshiro, Hiromichi Yamamoto, Norio Hayashi, Katsuhiro Kimura, Hiroaki Miwa, Shinji Igarashi, Kentaro Kline, Zoey Bouvet, Michael Singh, Shree Ram Tsuchiya, Hiroyuki Hoffman, Robert M.
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title_sort	pioglitazone, an agonist of pparγ, reverses doxorubicin-resistance in an osteosarcoma patient-derived orthotopic xenograft model by downregulating p-glycoprotein expression
title_auth	Pioglitazone, an agonist of PPARγ, reverses doxorubicin-resistance in an osteosarcoma patient-derived orthotopic xenograft model by downregulating P-glycoprotein expression
abstract	Multidrug resistance (MDR) which results in chemoresistance is a major problem in osteosarcoma. P-glycoprotein (P-gp) plays a critical role in MDR by pumping out chemotherapy agents. Peroxisome proliferator activated receptor gamma (PPARγ) is a nuclear receptor involved in cellular differentiation and proliferation. Recently, a correlation between the expression and activity of PPARγ and the expression of P-gp-associated with MDR, has been reported in several human cancers. The present study determined if pioglitazone (PIO), a PPARγ agonist, could modulate P-gp and overcome doxorubicin (DOX)-resistance in a patient-derived orthotopic xenograft (PDOX) model of osteosarcoma. P-gp mRNA expression was quantified in 143B human osteosarcoma cells treated with DOX with/without PIO. The osteosarcoma PDOX models were randomized into four treatment groups of six mice: Control; PIO alone; DOX alone; DOX and PIO combination. Tumor size and body weight were measured during the 14 days of treatment. DOX significantly induced P-gp mRNA in a dose-dependent manner in 143B cells. PIO inhibited the increase of P-gp mRNA induced by DOX treatment when co-administrated with DOX. Tumor growth was inhibited the most by the DOX-PIO combination. Tumors treated with the DOX-PIO combination also had the most tumor necrosis. This study suggests that the DOX-PIO combination could be used in the clinic for osteosarcoma patients who develop DOX-resistance.
abstractGer	Multidrug resistance (MDR) which results in chemoresistance is a major problem in osteosarcoma. P-glycoprotein (P-gp) plays a critical role in MDR by pumping out chemotherapy agents. Peroxisome proliferator activated receptor gamma (PPARγ) is a nuclear receptor involved in cellular differentiation and proliferation. Recently, a correlation between the expression and activity of PPARγ and the expression of P-gp-associated with MDR, has been reported in several human cancers. The present study determined if pioglitazone (PIO), a PPARγ agonist, could modulate P-gp and overcome doxorubicin (DOX)-resistance in a patient-derived orthotopic xenograft (PDOX) model of osteosarcoma. P-gp mRNA expression was quantified in 143B human osteosarcoma cells treated with DOX with/without PIO. The osteosarcoma PDOX models were randomized into four treatment groups of six mice: Control; PIO alone; DOX alone; DOX and PIO combination. Tumor size and body weight were measured during the 14 days of treatment. DOX significantly induced P-gp mRNA in a dose-dependent manner in 143B cells. PIO inhibited the increase of P-gp mRNA induced by DOX treatment when co-administrated with DOX. Tumor growth was inhibited the most by the DOX-PIO combination. Tumors treated with the DOX-PIO combination also had the most tumor necrosis. This study suggests that the DOX-PIO combination could be used in the clinic for osteosarcoma patients who develop DOX-resistance.
abstract_unstemmed	Multidrug resistance (MDR) which results in chemoresistance is a major problem in osteosarcoma. P-glycoprotein (P-gp) plays a critical role in MDR by pumping out chemotherapy agents. Peroxisome proliferator activated receptor gamma (PPARγ) is a nuclear receptor involved in cellular differentiation and proliferation. Recently, a correlation between the expression and activity of PPARγ and the expression of P-gp-associated with MDR, has been reported in several human cancers. The present study determined if pioglitazone (PIO), a PPARγ agonist, could modulate P-gp and overcome doxorubicin (DOX)-resistance in a patient-derived orthotopic xenograft (PDOX) model of osteosarcoma. P-gp mRNA expression was quantified in 143B human osteosarcoma cells treated with DOX with/without PIO. The osteosarcoma PDOX models were randomized into four treatment groups of six mice: Control; PIO alone; DOX alone; DOX and PIO combination. Tumor size and body weight were measured during the 14 days of treatment. DOX significantly induced P-gp mRNA in a dose-dependent manner in 143B cells. PIO inhibited the increase of P-gp mRNA induced by DOX treatment when co-administrated with DOX. Tumor growth was inhibited the most by the DOX-PIO combination. Tumors treated with the DOX-PIO combination also had the most tumor necrosis. This study suggests that the DOX-PIO combination could be used in the clinic for osteosarcoma patients who develop DOX-resistance.
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title_short	Pioglitazone, an agonist of PPARγ, reverses doxorubicin-resistance in an osteosarcoma patient-derived orthotopic xenograft model by downregulating P-glycoprotein expression
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author2	Sugisawa, Norihiko Miyake, Kentaro Oshiro, Hiromichi Yamamoto, Norio Hayashi, Katsuhiro Kimura, Hiroaki Miwa, Shinji Igarashi, Kentaro Kline, Zoey Bouvet, Michael Singh, Shree Ram Tsuchiya, Hiroyuki Hoffman, Robert M.
author2Str	Sugisawa, Norihiko Miyake, Kentaro Oshiro, Hiromichi Yamamoto, Norio Hayashi, Katsuhiro Kimura, Hiroaki Miwa, Shinji Igarashi, Kentaro Kline, Zoey Bouvet, Michael Singh, Shree Ram Tsuchiya, Hiroyuki Hoffman, Robert M.
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up_date	2024-07-06T17:47:13.011Z
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Pioglitazone, an agonist of PPARγ, reverses doxorubicin-resistance in an osteosarcoma patient-derived orthotopic xenograft model by downregulating P-glycoprotein expression

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