Imatinib mesylate inhibits androgen-independent PC-3 cell viability, proliferation, migration, and tumor growth by targeting platelet-derived growth factor receptor-α

Aim: The abnormal expression of oncogenic tyrosine kinase receptors such as platelet-derived growth factor receptors (PDGFRs) has been reported in cancer progression. However, the role of PDGFRs in the human androgen-independent prostate cancer PC-3 cell line is not well understood. Thus, this study...
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Gespeichert in:

Autor*in:	Nayeem, Md Junayed [verfasserIn] Yamamura, Aya [verfasserIn] Hayashi, Hisaki [verfasserIn] Muramatsu, Hiroyuki [verfasserIn] Nakamura, Kogenta [verfasserIn] Sassa, Naoto [verfasserIn] Sato, Motohiko [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2021

Schlagwörter:	PDGFR Prostate cancer Imatinib Androgen-independent

Übergeordnetes Werk:	Enthalten in: Life sciences - New York, NY [u.a.] : Elsevier Science, 1963, 288
Übergeordnetes Werk:	volume:288

DOI / URN:	10.1016/j.lfs.2021.120171

Katalog-ID:	ELV056262442

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allfields	10.1016/j.lfs.2021.120171 doi (DE-627)ELV056262442 (ELSEVIER)S0024-3205(21)01158-9 DE-627 ger DE-627 rda eng 570 VZ BIODIV DE-30 fid 42.00 bkl 44.40 bkl Nayeem, Md Junayed verfasserin aut Imatinib mesylate inhibits androgen-independent PC-3 cell viability, proliferation, migration, and tumor growth by targeting platelet-derived growth factor receptor-α 2021 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Aim: The abnormal expression of oncogenic tyrosine kinase receptors such as platelet-derived growth factor receptors (PDGFRs) has been reported in cancer progression. However, the role of PDGFRs in the human androgen-independent prostate cancer PC-3 cell line is not well understood. Thus, this study examined the role of PDGFRs in androgen-independent PC-3 cells.Main methods: PDGFR mRNA and protein expression was determined by quantitative real-time PCR and western blotting, respectively. The effects of the tyrosine kinase inhibitor imatinib (imatinib mesylate) and small interfering RNAs (siRNAs) were determined by a Cell Counting Kit-8 assay, bromodeoxyuridine assay, and Transwell migration assay. The in vivo effect of imatinib was analyzed using a tumor formation assay in nude mice.Key findings: PDGFRα was upregulated in androgen-independent PC-3 cells compared with normal prostate epithelial cells. PDGF-BB induced the phosphorylation of PDGFRα and downstream signaling molecules, including Akt, in a dose-dependent manner. Imatinib reduced the phosphorylation of the PDGFRα/Akt axis. Imatinib also suppressed the viability, proliferation, migration, and tumor growth of PC-3 cells. PDGFRα knockdown by siRNA decreased the viability and migration of PC-3 cells.Significance: These results demonstrated the distinct contribution of PDGFRα signaling to the proliferation and migration of PC-3 cells and suggested the potential for PDGFRα as a therapeutic target for metastatic and androgen-independent prostate cancer. PDGFR Prostate cancer Imatinib Androgen-independent Yamamura, Aya verfasserin aut Hayashi, Hisaki verfasserin aut Muramatsu, Hiroyuki verfasserin aut Nakamura, Kogenta verfasserin aut Sassa, Naoto verfasserin aut Sato, Motohiko verfasserin aut Enthalten in Life sciences New York, NY [u.a.] : Elsevier Science, 1963 288 Online-Ressource (DE-627)320515605 (DE-600)2013911-1 (DE-576)09095503X 1879-0631 nnns volume:288 GBV_USEFLAG_U GBV_ELV SYSFLAG_U FID-BIODIV SSG-OLC-PHA SSG-OPC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_224 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2143 GBV_ILN_2153 GBV_ILN_2336 GBV_ILN_4037 GBV_ILN_4242 GBV_ILN_4251 GBV_ILN_4313 GBV_ILN_4326 GBV_ILN_4334 GBV_ILN_4338 42.00 Biologie: Allgemeines VZ 44.40 Pharmazie Pharmazeutika VZ AR 288
spelling	10.1016/j.lfs.2021.120171 doi (DE-627)ELV056262442 (ELSEVIER)S0024-3205(21)01158-9 DE-627 ger DE-627 rda eng 570 VZ BIODIV DE-30 fid 42.00 bkl 44.40 bkl Nayeem, Md Junayed verfasserin aut Imatinib mesylate inhibits androgen-independent PC-3 cell viability, proliferation, migration, and tumor growth by targeting platelet-derived growth factor receptor-α 2021 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Aim: The abnormal expression of oncogenic tyrosine kinase receptors such as platelet-derived growth factor receptors (PDGFRs) has been reported in cancer progression. However, the role of PDGFRs in the human androgen-independent prostate cancer PC-3 cell line is not well understood. Thus, this study examined the role of PDGFRs in androgen-independent PC-3 cells.Main methods: PDGFR mRNA and protein expression was determined by quantitative real-time PCR and western blotting, respectively. The effects of the tyrosine kinase inhibitor imatinib (imatinib mesylate) and small interfering RNAs (siRNAs) were determined by a Cell Counting Kit-8 assay, bromodeoxyuridine assay, and Transwell migration assay. The in vivo effect of imatinib was analyzed using a tumor formation assay in nude mice.Key findings: PDGFRα was upregulated in androgen-independent PC-3 cells compared with normal prostate epithelial cells. PDGF-BB induced the phosphorylation of PDGFRα and downstream signaling molecules, including Akt, in a dose-dependent manner. Imatinib reduced the phosphorylation of the PDGFRα/Akt axis. Imatinib also suppressed the viability, proliferation, migration, and tumor growth of PC-3 cells. PDGFRα knockdown by siRNA decreased the viability and migration of PC-3 cells.Significance: These results demonstrated the distinct contribution of PDGFRα signaling to the proliferation and migration of PC-3 cells and suggested the potential for PDGFRα as a therapeutic target for metastatic and androgen-independent prostate cancer. PDGFR Prostate cancer Imatinib Androgen-independent Yamamura, Aya verfasserin aut Hayashi, Hisaki verfasserin aut Muramatsu, Hiroyuki verfasserin aut Nakamura, Kogenta verfasserin aut Sassa, Naoto verfasserin aut Sato, Motohiko verfasserin aut Enthalten in Life sciences New York, NY [u.a.] : Elsevier Science, 1963 288 Online-Ressource (DE-627)320515605 (DE-600)2013911-1 (DE-576)09095503X 1879-0631 nnns volume:288 GBV_USEFLAG_U GBV_ELV SYSFLAG_U FID-BIODIV SSG-OLC-PHA SSG-OPC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_224 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2143 GBV_ILN_2153 GBV_ILN_2336 GBV_ILN_4037 GBV_ILN_4242 GBV_ILN_4251 GBV_ILN_4313 GBV_ILN_4326 GBV_ILN_4334 GBV_ILN_4338 42.00 Biologie: Allgemeines VZ 44.40 Pharmazie Pharmazeutika VZ AR 288
allfields_unstemmed	10.1016/j.lfs.2021.120171 doi (DE-627)ELV056262442 (ELSEVIER)S0024-3205(21)01158-9 DE-627 ger DE-627 rda eng 570 VZ BIODIV DE-30 fid 42.00 bkl 44.40 bkl Nayeem, Md Junayed verfasserin aut Imatinib mesylate inhibits androgen-independent PC-3 cell viability, proliferation, migration, and tumor growth by targeting platelet-derived growth factor receptor-α 2021 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Aim: The abnormal expression of oncogenic tyrosine kinase receptors such as platelet-derived growth factor receptors (PDGFRs) has been reported in cancer progression. However, the role of PDGFRs in the human androgen-independent prostate cancer PC-3 cell line is not well understood. Thus, this study examined the role of PDGFRs in androgen-independent PC-3 cells.Main methods: PDGFR mRNA and protein expression was determined by quantitative real-time PCR and western blotting, respectively. The effects of the tyrosine kinase inhibitor imatinib (imatinib mesylate) and small interfering RNAs (siRNAs) were determined by a Cell Counting Kit-8 assay, bromodeoxyuridine assay, and Transwell migration assay. The in vivo effect of imatinib was analyzed using a tumor formation assay in nude mice.Key findings: PDGFRα was upregulated in androgen-independent PC-3 cells compared with normal prostate epithelial cells. PDGF-BB induced the phosphorylation of PDGFRα and downstream signaling molecules, including Akt, in a dose-dependent manner. Imatinib reduced the phosphorylation of the PDGFRα/Akt axis. Imatinib also suppressed the viability, proliferation, migration, and tumor growth of PC-3 cells. PDGFRα knockdown by siRNA decreased the viability and migration of PC-3 cells.Significance: These results demonstrated the distinct contribution of PDGFRα signaling to the proliferation and migration of PC-3 cells and suggested the potential for PDGFRα as a therapeutic target for metastatic and androgen-independent prostate cancer. PDGFR Prostate cancer Imatinib Androgen-independent Yamamura, Aya verfasserin aut Hayashi, Hisaki verfasserin aut Muramatsu, Hiroyuki verfasserin aut Nakamura, Kogenta verfasserin aut Sassa, Naoto verfasserin aut Sato, Motohiko verfasserin aut Enthalten in Life sciences New York, NY [u.a.] : Elsevier Science, 1963 288 Online-Ressource (DE-627)320515605 (DE-600)2013911-1 (DE-576)09095503X 1879-0631 nnns volume:288 GBV_USEFLAG_U GBV_ELV SYSFLAG_U FID-BIODIV SSG-OLC-PHA SSG-OPC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_224 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2143 GBV_ILN_2153 GBV_ILN_2336 GBV_ILN_4037 GBV_ILN_4242 GBV_ILN_4251 GBV_ILN_4313 GBV_ILN_4326 GBV_ILN_4334 GBV_ILN_4338 42.00 Biologie: Allgemeines VZ 44.40 Pharmazie Pharmazeutika VZ AR 288
allfieldsGer	10.1016/j.lfs.2021.120171 doi (DE-627)ELV056262442 (ELSEVIER)S0024-3205(21)01158-9 DE-627 ger DE-627 rda eng 570 VZ BIODIV DE-30 fid 42.00 bkl 44.40 bkl Nayeem, Md Junayed verfasserin aut Imatinib mesylate inhibits androgen-independent PC-3 cell viability, proliferation, migration, and tumor growth by targeting platelet-derived growth factor receptor-α 2021 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Aim: The abnormal expression of oncogenic tyrosine kinase receptors such as platelet-derived growth factor receptors (PDGFRs) has been reported in cancer progression. However, the role of PDGFRs in the human androgen-independent prostate cancer PC-3 cell line is not well understood. Thus, this study examined the role of PDGFRs in androgen-independent PC-3 cells.Main methods: PDGFR mRNA and protein expression was determined by quantitative real-time PCR and western blotting, respectively. The effects of the tyrosine kinase inhibitor imatinib (imatinib mesylate) and small interfering RNAs (siRNAs) were determined by a Cell Counting Kit-8 assay, bromodeoxyuridine assay, and Transwell migration assay. The in vivo effect of imatinib was analyzed using a tumor formation assay in nude mice.Key findings: PDGFRα was upregulated in androgen-independent PC-3 cells compared with normal prostate epithelial cells. PDGF-BB induced the phosphorylation of PDGFRα and downstream signaling molecules, including Akt, in a dose-dependent manner. Imatinib reduced the phosphorylation of the PDGFRα/Akt axis. Imatinib also suppressed the viability, proliferation, migration, and tumor growth of PC-3 cells. PDGFRα knockdown by siRNA decreased the viability and migration of PC-3 cells.Significance: These results demonstrated the distinct contribution of PDGFRα signaling to the proliferation and migration of PC-3 cells and suggested the potential for PDGFRα as a therapeutic target for metastatic and androgen-independent prostate cancer. PDGFR Prostate cancer Imatinib Androgen-independent Yamamura, Aya verfasserin aut Hayashi, Hisaki verfasserin aut Muramatsu, Hiroyuki verfasserin aut Nakamura, Kogenta verfasserin aut Sassa, Naoto verfasserin aut Sato, Motohiko verfasserin aut Enthalten in Life sciences New York, NY [u.a.] : Elsevier Science, 1963 288 Online-Ressource (DE-627)320515605 (DE-600)2013911-1 (DE-576)09095503X 1879-0631 nnns volume:288 GBV_USEFLAG_U GBV_ELV SYSFLAG_U FID-BIODIV SSG-OLC-PHA SSG-OPC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_224 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2143 GBV_ILN_2153 GBV_ILN_2336 GBV_ILN_4037 GBV_ILN_4242 GBV_ILN_4251 GBV_ILN_4313 GBV_ILN_4326 GBV_ILN_4334 GBV_ILN_4338 42.00 Biologie: Allgemeines VZ 44.40 Pharmazie Pharmazeutika VZ AR 288
allfieldsSound	10.1016/j.lfs.2021.120171 doi (DE-627)ELV056262442 (ELSEVIER)S0024-3205(21)01158-9 DE-627 ger DE-627 rda eng 570 VZ BIODIV DE-30 fid 42.00 bkl 44.40 bkl Nayeem, Md Junayed verfasserin aut Imatinib mesylate inhibits androgen-independent PC-3 cell viability, proliferation, migration, and tumor growth by targeting platelet-derived growth factor receptor-α 2021 nicht spezifiziert zzz rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Aim: The abnormal expression of oncogenic tyrosine kinase receptors such as platelet-derived growth factor receptors (PDGFRs) has been reported in cancer progression. However, the role of PDGFRs in the human androgen-independent prostate cancer PC-3 cell line is not well understood. Thus, this study examined the role of PDGFRs in androgen-independent PC-3 cells.Main methods: PDGFR mRNA and protein expression was determined by quantitative real-time PCR and western blotting, respectively. The effects of the tyrosine kinase inhibitor imatinib (imatinib mesylate) and small interfering RNAs (siRNAs) were determined by a Cell Counting Kit-8 assay, bromodeoxyuridine assay, and Transwell migration assay. The in vivo effect of imatinib was analyzed using a tumor formation assay in nude mice.Key findings: PDGFRα was upregulated in androgen-independent PC-3 cells compared with normal prostate epithelial cells. PDGF-BB induced the phosphorylation of PDGFRα and downstream signaling molecules, including Akt, in a dose-dependent manner. Imatinib reduced the phosphorylation of the PDGFRα/Akt axis. Imatinib also suppressed the viability, proliferation, migration, and tumor growth of PC-3 cells. PDGFRα knockdown by siRNA decreased the viability and migration of PC-3 cells.Significance: These results demonstrated the distinct contribution of PDGFRα signaling to the proliferation and migration of PC-3 cells and suggested the potential for PDGFRα as a therapeutic target for metastatic and androgen-independent prostate cancer. PDGFR Prostate cancer Imatinib Androgen-independent Yamamura, Aya verfasserin aut Hayashi, Hisaki verfasserin aut Muramatsu, Hiroyuki verfasserin aut Nakamura, Kogenta verfasserin aut Sassa, Naoto verfasserin aut Sato, Motohiko verfasserin aut Enthalten in Life sciences New York, NY [u.a.] : Elsevier Science, 1963 288 Online-Ressource (DE-627)320515605 (DE-600)2013911-1 (DE-576)09095503X 1879-0631 nnns volume:288 GBV_USEFLAG_U GBV_ELV SYSFLAG_U FID-BIODIV SSG-OLC-PHA SSG-OPC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_224 GBV_ILN_370 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2034 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2143 GBV_ILN_2153 GBV_ILN_2336 GBV_ILN_4037 GBV_ILN_4242 GBV_ILN_4251 GBV_ILN_4313 GBV_ILN_4326 GBV_ILN_4334 GBV_ILN_4338 42.00 Biologie: Allgemeines VZ 44.40 Pharmazie Pharmazeutika VZ AR 288
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authorswithroles_txt_mv	Nayeem, Md Junayed @@aut@@ Yamamura, Aya @@aut@@ Hayashi, Hisaki @@aut@@ Muramatsu, Hiroyuki @@aut@@ Nakamura, Kogenta @@aut@@ Sassa, Naoto @@aut@@ Sato, Motohiko @@aut@@
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author	Nayeem, Md Junayed
spellingShingle	Nayeem, Md Junayed ddc 570 fid BIODIV bkl 42.00 bkl 44.40 misc PDGFR misc Prostate cancer misc Imatinib misc Androgen-independent Imatinib mesylate inhibits androgen-independent PC-3 cell viability, proliferation, migration, and tumor growth by targeting platelet-derived growth factor receptor-α
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topic_title	570 VZ BIODIV DE-30 fid 42.00 bkl 44.40 bkl Imatinib mesylate inhibits androgen-independent PC-3 cell viability, proliferation, migration, and tumor growth by targeting platelet-derived growth factor receptor-α PDGFR Prostate cancer Imatinib Androgen-independent
topic	ddc 570 fid BIODIV bkl 42.00 bkl 44.40 misc PDGFR misc Prostate cancer misc Imatinib misc Androgen-independent
topic_unstemmed	ddc 570 fid BIODIV bkl 42.00 bkl 44.40 misc PDGFR misc Prostate cancer misc Imatinib misc Androgen-independent
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title	Imatinib mesylate inhibits androgen-independent PC-3 cell viability, proliferation, migration, and tumor growth by targeting platelet-derived growth factor receptor-α
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title_full	Imatinib mesylate inhibits androgen-independent PC-3 cell viability, proliferation, migration, and tumor growth by targeting platelet-derived growth factor receptor-α
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author_browse	Nayeem, Md Junayed Yamamura, Aya Hayashi, Hisaki Muramatsu, Hiroyuki Nakamura, Kogenta Sassa, Naoto Sato, Motohiko
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title_sort	imatinib mesylate inhibits androgen-independent pc-3 cell viability, proliferation, migration, and tumor growth by targeting platelet-derived growth factor receptor-α
title_auth	Imatinib mesylate inhibits androgen-independent PC-3 cell viability, proliferation, migration, and tumor growth by targeting platelet-derived growth factor receptor-α
abstract	Aim: The abnormal expression of oncogenic tyrosine kinase receptors such as platelet-derived growth factor receptors (PDGFRs) has been reported in cancer progression. However, the role of PDGFRs in the human androgen-independent prostate cancer PC-3 cell line is not well understood. Thus, this study examined the role of PDGFRs in androgen-independent PC-3 cells.Main methods: PDGFR mRNA and protein expression was determined by quantitative real-time PCR and western blotting, respectively. The effects of the tyrosine kinase inhibitor imatinib (imatinib mesylate) and small interfering RNAs (siRNAs) were determined by a Cell Counting Kit-8 assay, bromodeoxyuridine assay, and Transwell migration assay. The in vivo effect of imatinib was analyzed using a tumor formation assay in nude mice.Key findings: PDGFRα was upregulated in androgen-independent PC-3 cells compared with normal prostate epithelial cells. PDGF-BB induced the phosphorylation of PDGFRα and downstream signaling molecules, including Akt, in a dose-dependent manner. Imatinib reduced the phosphorylation of the PDGFRα/Akt axis. Imatinib also suppressed the viability, proliferation, migration, and tumor growth of PC-3 cells. PDGFRα knockdown by siRNA decreased the viability and migration of PC-3 cells.Significance: These results demonstrated the distinct contribution of PDGFRα signaling to the proliferation and migration of PC-3 cells and suggested the potential for PDGFRα as a therapeutic target for metastatic and androgen-independent prostate cancer.
abstractGer	Aim: The abnormal expression of oncogenic tyrosine kinase receptors such as platelet-derived growth factor receptors (PDGFRs) has been reported in cancer progression. However, the role of PDGFRs in the human androgen-independent prostate cancer PC-3 cell line is not well understood. Thus, this study examined the role of PDGFRs in androgen-independent PC-3 cells.Main methods: PDGFR mRNA and protein expression was determined by quantitative real-time PCR and western blotting, respectively. The effects of the tyrosine kinase inhibitor imatinib (imatinib mesylate) and small interfering RNAs (siRNAs) were determined by a Cell Counting Kit-8 assay, bromodeoxyuridine assay, and Transwell migration assay. The in vivo effect of imatinib was analyzed using a tumor formation assay in nude mice.Key findings: PDGFRα was upregulated in androgen-independent PC-3 cells compared with normal prostate epithelial cells. PDGF-BB induced the phosphorylation of PDGFRα and downstream signaling molecules, including Akt, in a dose-dependent manner. Imatinib reduced the phosphorylation of the PDGFRα/Akt axis. Imatinib also suppressed the viability, proliferation, migration, and tumor growth of PC-3 cells. PDGFRα knockdown by siRNA decreased the viability and migration of PC-3 cells.Significance: These results demonstrated the distinct contribution of PDGFRα signaling to the proliferation and migration of PC-3 cells and suggested the potential for PDGFRα as a therapeutic target for metastatic and androgen-independent prostate cancer.
abstract_unstemmed	Aim: The abnormal expression of oncogenic tyrosine kinase receptors such as platelet-derived growth factor receptors (PDGFRs) has been reported in cancer progression. However, the role of PDGFRs in the human androgen-independent prostate cancer PC-3 cell line is not well understood. Thus, this study examined the role of PDGFRs in androgen-independent PC-3 cells.Main methods: PDGFR mRNA and protein expression was determined by quantitative real-time PCR and western blotting, respectively. The effects of the tyrosine kinase inhibitor imatinib (imatinib mesylate) and small interfering RNAs (siRNAs) were determined by a Cell Counting Kit-8 assay, bromodeoxyuridine assay, and Transwell migration assay. The in vivo effect of imatinib was analyzed using a tumor formation assay in nude mice.Key findings: PDGFRα was upregulated in androgen-independent PC-3 cells compared with normal prostate epithelial cells. PDGF-BB induced the phosphorylation of PDGFRα and downstream signaling molecules, including Akt, in a dose-dependent manner. Imatinib reduced the phosphorylation of the PDGFRα/Akt axis. Imatinib also suppressed the viability, proliferation, migration, and tumor growth of PC-3 cells. PDGFRα knockdown by siRNA decreased the viability and migration of PC-3 cells.Significance: These results demonstrated the distinct contribution of PDGFRα signaling to the proliferation and migration of PC-3 cells and suggested the potential for PDGFRα as a therapeutic target for metastatic and androgen-independent prostate cancer.
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title_short	Imatinib mesylate inhibits androgen-independent PC-3 cell viability, proliferation, migration, and tumor growth by targeting platelet-derived growth factor receptor-α
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author2	Yamamura, Aya Hayashi, Hisaki Muramatsu, Hiroyuki Nakamura, Kogenta Sassa, Naoto Sato, Motohiko
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doi_str	10.1016/j.lfs.2021.120171
up_date	2024-07-06T19:53:22.800Z
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Imatinib mesylate inhibits androgen-independent PC-3 cell viability, proliferation, migration, and tumor growth by targeting platelet-derived growth factor receptor-α

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