Targeting prolyl isomerase Pin1 as a promising strategy to overcome resistance to cancer therapies
The development of tumor therapeutic resistance is one of the important reasons for the failure of antitumor therapy. Starting with multiple targets and multiple signaling pathways is helpful in understanding the mechanism of tumor resistance. The overexpression of prolyl isomerase Pin1 is highly co...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Wu, Wenda [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2022transfer abstract |
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| Schlagwörter: |
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| Übergeordnetes Werk: |
Enthalten in: Social insurance premiums and corporate cash holdings: Evidence from social insurance law in China - Deng, Lixing ELSEVIER, 2022, the official journal of the Italian Pharmacological Society, London |
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| Übergeordnetes Werk: |
volume:184 ; year:2022 ; pages:0 |
| Links: |
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| DOI / URN: |
10.1016/j.phrs.2022.106456 |
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ELV059148152 |
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| 520 | |a The development of tumor therapeutic resistance is one of the important reasons for the failure of antitumor therapy. Starting with multiple targets and multiple signaling pathways is helpful in understanding the mechanism of tumor resistance. The overexpression of prolyl isomerase Pin1 is highly correlated with the malignancy of cancer, since Pin1 controls many oncogenes and tumor suppressors, as well as a variety of cancer-driving signaling pathways. Strikingly, numerous studies have shown that Pin1 is directly involved in therapeutic resistance. In this review, we mainly summarize the functions and mechanisms of Pin1 in therapeutic resistance of multifarious cancers, such as breast, liver, and pancreatic carcinomas. Furtherly, from the perspective of Pin1-driven cancer signaling pathways including Raf/MEK/ERK, PI3K/Akt, Wnt/β-catenin, NF-κB, as well as Pin1 inhibitors containing juglone, epigallocatechin-3-gallate (EGCG), all-trans retinoic acid (ATRA) and arsenic trioxide (ATO), it is better to demonstrate the important potential role and mechanism of Pin1 in resistance and sensitization to cancer therapies. It will provide new therapeutic approaches for clinical reversal and prevention of tumor resistance by employing synergistic administration of Pin1 inhibitors and chemotherapeutics, implementing combination therapy of Pin1-related cancer signaling pathway inhibitors and Pin1 inhibitors, and exploiting novel Pin1-specific inhibitors. | ||
| 520 | |a The development of tumor therapeutic resistance is one of the important reasons for the failure of antitumor therapy. Starting with multiple targets and multiple signaling pathways is helpful in understanding the mechanism of tumor resistance. The overexpression of prolyl isomerase Pin1 is highly correlated with the malignancy of cancer, since Pin1 controls many oncogenes and tumor suppressors, as well as a variety of cancer-driving signaling pathways. Strikingly, numerous studies have shown that Pin1 is directly involved in therapeutic resistance. In this review, we mainly summarize the functions and mechanisms of Pin1 in therapeutic resistance of multifarious cancers, such as breast, liver, and pancreatic carcinomas. Furtherly, from the perspective of Pin1-driven cancer signaling pathways including Raf/MEK/ERK, PI3K/Akt, Wnt/β-catenin, NF-κB, as well as Pin1 inhibitors containing juglone, epigallocatechin-3-gallate (EGCG), all-trans retinoic acid (ATRA) and arsenic trioxide (ATO), it is better to demonstrate the important potential role and mechanism of Pin1 in resistance and sensitization to cancer therapies. It will provide new therapeutic approaches for clinical reversal and prevention of tumor resistance by employing synergistic administration of Pin1 inhibitors and chemotherapeutics, implementing combination therapy of Pin1-related cancer signaling pathway inhibitors and Pin1 inhibitors, and exploiting novel Pin1-specific inhibitors. | ||
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10.1016/j.phrs.2022.106456 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001925.pica (DE-627)ELV059148152 (ELSEVIER)S1043-6618(22)00402-9 DE-627 ger DE-627 rakwb eng 330 VZ Wu, Wenda verfasserin aut Targeting prolyl isomerase Pin1 as a promising strategy to overcome resistance to cancer therapies 2022transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier The development of tumor therapeutic resistance is one of the important reasons for the failure of antitumor therapy. Starting with multiple targets and multiple signaling pathways is helpful in understanding the mechanism of tumor resistance. The overexpression of prolyl isomerase Pin1 is highly correlated with the malignancy of cancer, since Pin1 controls many oncogenes and tumor suppressors, as well as a variety of cancer-driving signaling pathways. Strikingly, numerous studies have shown that Pin1 is directly involved in therapeutic resistance. In this review, we mainly summarize the functions and mechanisms of Pin1 in therapeutic resistance of multifarious cancers, such as breast, liver, and pancreatic carcinomas. Furtherly, from the perspective of Pin1-driven cancer signaling pathways including Raf/MEK/ERK, PI3K/Akt, Wnt/β-catenin, NF-κB, as well as Pin1 inhibitors containing juglone, epigallocatechin-3-gallate (EGCG), all-trans retinoic acid (ATRA) and arsenic trioxide (ATO), it is better to demonstrate the important potential role and mechanism of Pin1 in resistance and sensitization to cancer therapies. It will provide new therapeutic approaches for clinical reversal and prevention of tumor resistance by employing synergistic administration of Pin1 inhibitors and chemotherapeutics, implementing combination therapy of Pin1-related cancer signaling pathway inhibitors and Pin1 inhibitors, and exploiting novel Pin1-specific inhibitors. The development of tumor therapeutic resistance is one of the important reasons for the failure of antitumor therapy. Starting with multiple targets and multiple signaling pathways is helpful in understanding the mechanism of tumor resistance. The overexpression of prolyl isomerase Pin1 is highly correlated with the malignancy of cancer, since Pin1 controls many oncogenes and tumor suppressors, as well as a variety of cancer-driving signaling pathways. Strikingly, numerous studies have shown that Pin1 is directly involved in therapeutic resistance. In this review, we mainly summarize the functions and mechanisms of Pin1 in therapeutic resistance of multifarious cancers, such as breast, liver, and pancreatic carcinomas. Furtherly, from the perspective of Pin1-driven cancer signaling pathways including Raf/MEK/ERK, PI3K/Akt, Wnt/β-catenin, NF-κB, as well as Pin1 inhibitors containing juglone, epigallocatechin-3-gallate (EGCG), all-trans retinoic acid (ATRA) and arsenic trioxide (ATO), it is better to demonstrate the important potential role and mechanism of Pin1 in resistance and sensitization to cancer therapies. It will provide new therapeutic approaches for clinical reversal and prevention of tumor resistance by employing synergistic administration of Pin1 inhibitors and chemotherapeutics, implementing combination therapy of Pin1-related cancer signaling pathway inhibitors and Pin1 inhibitors, and exploiting novel Pin1-specific inhibitors. Ser/Thr-Pro Elsevier ALL Elsevier TAM Elsevier BCSCs Elsevier RKIP Elsevier PPIase Elsevier ADM Elsevier HIF-1α Elsevier UA Elsevier AP-1 Elsevier XPO5 Elsevier TNBC Elsevier CSCs Elsevier AML Elsevier BCRP Elsevier P-gp Elsevier TRAIL Elsevier EGCG Elsevier HCC Elsevier Tex10 Elsevier DOX Elsevier EMT Elsevier ER Elsevier AR Elsevier PDAC Elsevier CRC Elsevier EET Elsevier HNSCC Elsevier SMRT Elsevier ATRA Elsevier CRPC Elsevier HBx Elsevier FDA Elsevier VCR Elsevier EGFR Elsevier Hsp90 Elsevier IκB Elsevier CAFs Elsevier IRAK1 Elsevier TLR Elsevier TFAP2A Elsevier NSCLC Elsevier HIP1R Elsevier IKK Elsevier BIO Elsevier TME Elsevier PML Elsevier FAS Elsevier Pin1 Elsevier ATO Elsevier HER2 Elsevier APL Elsevier 5-FU Elsevier Xue, Xuezhen oth Chen, Yan oth Zheng, Ning oth Wang, Jichuang oth Enthalten in Academic Press Deng, Lixing ELSEVIER Social insurance premiums and corporate cash holdings: Evidence from social insurance law in China 2022 the official journal of the Italian Pharmacological Society London (DE-627)ELV008224951 volume:184 year:2022 pages:0 https://doi.org/10.1016/j.phrs.2022.106456 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U AR 184 2022 0 |
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10.1016/j.phrs.2022.106456 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001925.pica (DE-627)ELV059148152 (ELSEVIER)S1043-6618(22)00402-9 DE-627 ger DE-627 rakwb eng 330 VZ Wu, Wenda verfasserin aut Targeting prolyl isomerase Pin1 as a promising strategy to overcome resistance to cancer therapies 2022transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier The development of tumor therapeutic resistance is one of the important reasons for the failure of antitumor therapy. Starting with multiple targets and multiple signaling pathways is helpful in understanding the mechanism of tumor resistance. The overexpression of prolyl isomerase Pin1 is highly correlated with the malignancy of cancer, since Pin1 controls many oncogenes and tumor suppressors, as well as a variety of cancer-driving signaling pathways. Strikingly, numerous studies have shown that Pin1 is directly involved in therapeutic resistance. In this review, we mainly summarize the functions and mechanisms of Pin1 in therapeutic resistance of multifarious cancers, such as breast, liver, and pancreatic carcinomas. Furtherly, from the perspective of Pin1-driven cancer signaling pathways including Raf/MEK/ERK, PI3K/Akt, Wnt/β-catenin, NF-κB, as well as Pin1 inhibitors containing juglone, epigallocatechin-3-gallate (EGCG), all-trans retinoic acid (ATRA) and arsenic trioxide (ATO), it is better to demonstrate the important potential role and mechanism of Pin1 in resistance and sensitization to cancer therapies. It will provide new therapeutic approaches for clinical reversal and prevention of tumor resistance by employing synergistic administration of Pin1 inhibitors and chemotherapeutics, implementing combination therapy of Pin1-related cancer signaling pathway inhibitors and Pin1 inhibitors, and exploiting novel Pin1-specific inhibitors. The development of tumor therapeutic resistance is one of the important reasons for the failure of antitumor therapy. Starting with multiple targets and multiple signaling pathways is helpful in understanding the mechanism of tumor resistance. The overexpression of prolyl isomerase Pin1 is highly correlated with the malignancy of cancer, since Pin1 controls many oncogenes and tumor suppressors, as well as a variety of cancer-driving signaling pathways. Strikingly, numerous studies have shown that Pin1 is directly involved in therapeutic resistance. In this review, we mainly summarize the functions and mechanisms of Pin1 in therapeutic resistance of multifarious cancers, such as breast, liver, and pancreatic carcinomas. Furtherly, from the perspective of Pin1-driven cancer signaling pathways including Raf/MEK/ERK, PI3K/Akt, Wnt/β-catenin, NF-κB, as well as Pin1 inhibitors containing juglone, epigallocatechin-3-gallate (EGCG), all-trans retinoic acid (ATRA) and arsenic trioxide (ATO), it is better to demonstrate the important potential role and mechanism of Pin1 in resistance and sensitization to cancer therapies. It will provide new therapeutic approaches for clinical reversal and prevention of tumor resistance by employing synergistic administration of Pin1 inhibitors and chemotherapeutics, implementing combination therapy of Pin1-related cancer signaling pathway inhibitors and Pin1 inhibitors, and exploiting novel Pin1-specific inhibitors. Ser/Thr-Pro Elsevier ALL Elsevier TAM Elsevier BCSCs Elsevier RKIP Elsevier PPIase Elsevier ADM Elsevier HIF-1α Elsevier UA Elsevier AP-1 Elsevier XPO5 Elsevier TNBC Elsevier CSCs Elsevier AML Elsevier BCRP Elsevier P-gp Elsevier TRAIL Elsevier EGCG Elsevier HCC Elsevier Tex10 Elsevier DOX Elsevier EMT Elsevier ER Elsevier AR Elsevier PDAC Elsevier CRC Elsevier EET Elsevier HNSCC Elsevier SMRT Elsevier ATRA Elsevier CRPC Elsevier HBx Elsevier FDA Elsevier VCR Elsevier EGFR Elsevier Hsp90 Elsevier IκB Elsevier CAFs Elsevier IRAK1 Elsevier TLR Elsevier TFAP2A Elsevier NSCLC Elsevier HIP1R Elsevier IKK Elsevier BIO Elsevier TME Elsevier PML Elsevier FAS Elsevier Pin1 Elsevier ATO Elsevier HER2 Elsevier APL Elsevier 5-FU Elsevier Xue, Xuezhen oth Chen, Yan oth Zheng, Ning oth Wang, Jichuang oth Enthalten in Academic Press Deng, Lixing ELSEVIER Social insurance premiums and corporate cash holdings: Evidence from social insurance law in China 2022 the official journal of the Italian Pharmacological Society London (DE-627)ELV008224951 volume:184 year:2022 pages:0 https://doi.org/10.1016/j.phrs.2022.106456 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U AR 184 2022 0 |
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10.1016/j.phrs.2022.106456 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001925.pica (DE-627)ELV059148152 (ELSEVIER)S1043-6618(22)00402-9 DE-627 ger DE-627 rakwb eng 330 VZ Wu, Wenda verfasserin aut Targeting prolyl isomerase Pin1 as a promising strategy to overcome resistance to cancer therapies 2022transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier The development of tumor therapeutic resistance is one of the important reasons for the failure of antitumor therapy. Starting with multiple targets and multiple signaling pathways is helpful in understanding the mechanism of tumor resistance. The overexpression of prolyl isomerase Pin1 is highly correlated with the malignancy of cancer, since Pin1 controls many oncogenes and tumor suppressors, as well as a variety of cancer-driving signaling pathways. Strikingly, numerous studies have shown that Pin1 is directly involved in therapeutic resistance. In this review, we mainly summarize the functions and mechanisms of Pin1 in therapeutic resistance of multifarious cancers, such as breast, liver, and pancreatic carcinomas. Furtherly, from the perspective of Pin1-driven cancer signaling pathways including Raf/MEK/ERK, PI3K/Akt, Wnt/β-catenin, NF-κB, as well as Pin1 inhibitors containing juglone, epigallocatechin-3-gallate (EGCG), all-trans retinoic acid (ATRA) and arsenic trioxide (ATO), it is better to demonstrate the important potential role and mechanism of Pin1 in resistance and sensitization to cancer therapies. It will provide new therapeutic approaches for clinical reversal and prevention of tumor resistance by employing synergistic administration of Pin1 inhibitors and chemotherapeutics, implementing combination therapy of Pin1-related cancer signaling pathway inhibitors and Pin1 inhibitors, and exploiting novel Pin1-specific inhibitors. The development of tumor therapeutic resistance is one of the important reasons for the failure of antitumor therapy. Starting with multiple targets and multiple signaling pathways is helpful in understanding the mechanism of tumor resistance. The overexpression of prolyl isomerase Pin1 is highly correlated with the malignancy of cancer, since Pin1 controls many oncogenes and tumor suppressors, as well as a variety of cancer-driving signaling pathways. Strikingly, numerous studies have shown that Pin1 is directly involved in therapeutic resistance. In this review, we mainly summarize the functions and mechanisms of Pin1 in therapeutic resistance of multifarious cancers, such as breast, liver, and pancreatic carcinomas. Furtherly, from the perspective of Pin1-driven cancer signaling pathways including Raf/MEK/ERK, PI3K/Akt, Wnt/β-catenin, NF-κB, as well as Pin1 inhibitors containing juglone, epigallocatechin-3-gallate (EGCG), all-trans retinoic acid (ATRA) and arsenic trioxide (ATO), it is better to demonstrate the important potential role and mechanism of Pin1 in resistance and sensitization to cancer therapies. It will provide new therapeutic approaches for clinical reversal and prevention of tumor resistance by employing synergistic administration of Pin1 inhibitors and chemotherapeutics, implementing combination therapy of Pin1-related cancer signaling pathway inhibitors and Pin1 inhibitors, and exploiting novel Pin1-specific inhibitors. Ser/Thr-Pro Elsevier ALL Elsevier TAM Elsevier BCSCs Elsevier RKIP Elsevier PPIase Elsevier ADM Elsevier HIF-1α Elsevier UA Elsevier AP-1 Elsevier XPO5 Elsevier TNBC Elsevier CSCs Elsevier AML Elsevier BCRP Elsevier P-gp Elsevier TRAIL Elsevier EGCG Elsevier HCC Elsevier Tex10 Elsevier DOX Elsevier EMT Elsevier ER Elsevier AR Elsevier PDAC Elsevier CRC Elsevier EET Elsevier HNSCC Elsevier SMRT Elsevier ATRA Elsevier CRPC Elsevier HBx Elsevier FDA Elsevier VCR Elsevier EGFR Elsevier Hsp90 Elsevier IκB Elsevier CAFs Elsevier IRAK1 Elsevier TLR Elsevier TFAP2A Elsevier NSCLC Elsevier HIP1R Elsevier IKK Elsevier BIO Elsevier TME Elsevier PML Elsevier FAS Elsevier Pin1 Elsevier ATO Elsevier HER2 Elsevier APL Elsevier 5-FU Elsevier Xue, Xuezhen oth Chen, Yan oth Zheng, Ning oth Wang, Jichuang oth Enthalten in Academic Press Deng, Lixing ELSEVIER Social insurance premiums and corporate cash holdings: Evidence from social insurance law in China 2022 the official journal of the Italian Pharmacological Society London (DE-627)ELV008224951 volume:184 year:2022 pages:0 https://doi.org/10.1016/j.phrs.2022.106456 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U AR 184 2022 0 |
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10.1016/j.phrs.2022.106456 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001925.pica (DE-627)ELV059148152 (ELSEVIER)S1043-6618(22)00402-9 DE-627 ger DE-627 rakwb eng 330 VZ Wu, Wenda verfasserin aut Targeting prolyl isomerase Pin1 as a promising strategy to overcome resistance to cancer therapies 2022transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier The development of tumor therapeutic resistance is one of the important reasons for the failure of antitumor therapy. Starting with multiple targets and multiple signaling pathways is helpful in understanding the mechanism of tumor resistance. The overexpression of prolyl isomerase Pin1 is highly correlated with the malignancy of cancer, since Pin1 controls many oncogenes and tumor suppressors, as well as a variety of cancer-driving signaling pathways. Strikingly, numerous studies have shown that Pin1 is directly involved in therapeutic resistance. In this review, we mainly summarize the functions and mechanisms of Pin1 in therapeutic resistance of multifarious cancers, such as breast, liver, and pancreatic carcinomas. Furtherly, from the perspective of Pin1-driven cancer signaling pathways including Raf/MEK/ERK, PI3K/Akt, Wnt/β-catenin, NF-κB, as well as Pin1 inhibitors containing juglone, epigallocatechin-3-gallate (EGCG), all-trans retinoic acid (ATRA) and arsenic trioxide (ATO), it is better to demonstrate the important potential role and mechanism of Pin1 in resistance and sensitization to cancer therapies. It will provide new therapeutic approaches for clinical reversal and prevention of tumor resistance by employing synergistic administration of Pin1 inhibitors and chemotherapeutics, implementing combination therapy of Pin1-related cancer signaling pathway inhibitors and Pin1 inhibitors, and exploiting novel Pin1-specific inhibitors. The development of tumor therapeutic resistance is one of the important reasons for the failure of antitumor therapy. Starting with multiple targets and multiple signaling pathways is helpful in understanding the mechanism of tumor resistance. The overexpression of prolyl isomerase Pin1 is highly correlated with the malignancy of cancer, since Pin1 controls many oncogenes and tumor suppressors, as well as a variety of cancer-driving signaling pathways. Strikingly, numerous studies have shown that Pin1 is directly involved in therapeutic resistance. In this review, we mainly summarize the functions and mechanisms of Pin1 in therapeutic resistance of multifarious cancers, such as breast, liver, and pancreatic carcinomas. Furtherly, from the perspective of Pin1-driven cancer signaling pathways including Raf/MEK/ERK, PI3K/Akt, Wnt/β-catenin, NF-κB, as well as Pin1 inhibitors containing juglone, epigallocatechin-3-gallate (EGCG), all-trans retinoic acid (ATRA) and arsenic trioxide (ATO), it is better to demonstrate the important potential role and mechanism of Pin1 in resistance and sensitization to cancer therapies. It will provide new therapeutic approaches for clinical reversal and prevention of tumor resistance by employing synergistic administration of Pin1 inhibitors and chemotherapeutics, implementing combination therapy of Pin1-related cancer signaling pathway inhibitors and Pin1 inhibitors, and exploiting novel Pin1-specific inhibitors. Ser/Thr-Pro Elsevier ALL Elsevier TAM Elsevier BCSCs Elsevier RKIP Elsevier PPIase Elsevier ADM Elsevier HIF-1α Elsevier UA Elsevier AP-1 Elsevier XPO5 Elsevier TNBC Elsevier CSCs Elsevier AML Elsevier BCRP Elsevier P-gp Elsevier TRAIL Elsevier EGCG Elsevier HCC Elsevier Tex10 Elsevier DOX Elsevier EMT Elsevier ER Elsevier AR Elsevier PDAC Elsevier CRC Elsevier EET Elsevier HNSCC Elsevier SMRT Elsevier ATRA Elsevier CRPC Elsevier HBx Elsevier FDA Elsevier VCR Elsevier EGFR Elsevier Hsp90 Elsevier IκB Elsevier CAFs Elsevier IRAK1 Elsevier TLR Elsevier TFAP2A Elsevier NSCLC Elsevier HIP1R Elsevier IKK Elsevier BIO Elsevier TME Elsevier PML Elsevier FAS Elsevier Pin1 Elsevier ATO Elsevier HER2 Elsevier APL Elsevier 5-FU Elsevier Xue, Xuezhen oth Chen, Yan oth Zheng, Ning oth Wang, Jichuang oth Enthalten in Academic Press Deng, Lixing ELSEVIER Social insurance premiums and corporate cash holdings: Evidence from social insurance law in China 2022 the official journal of the Italian Pharmacological Society London (DE-627)ELV008224951 volume:184 year:2022 pages:0 https://doi.org/10.1016/j.phrs.2022.106456 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U AR 184 2022 0 |
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10.1016/j.phrs.2022.106456 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001925.pica (DE-627)ELV059148152 (ELSEVIER)S1043-6618(22)00402-9 DE-627 ger DE-627 rakwb eng 330 VZ Wu, Wenda verfasserin aut Targeting prolyl isomerase Pin1 as a promising strategy to overcome resistance to cancer therapies 2022transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier The development of tumor therapeutic resistance is one of the important reasons for the failure of antitumor therapy. Starting with multiple targets and multiple signaling pathways is helpful in understanding the mechanism of tumor resistance. The overexpression of prolyl isomerase Pin1 is highly correlated with the malignancy of cancer, since Pin1 controls many oncogenes and tumor suppressors, as well as a variety of cancer-driving signaling pathways. Strikingly, numerous studies have shown that Pin1 is directly involved in therapeutic resistance. In this review, we mainly summarize the functions and mechanisms of Pin1 in therapeutic resistance of multifarious cancers, such as breast, liver, and pancreatic carcinomas. Furtherly, from the perspective of Pin1-driven cancer signaling pathways including Raf/MEK/ERK, PI3K/Akt, Wnt/β-catenin, NF-κB, as well as Pin1 inhibitors containing juglone, epigallocatechin-3-gallate (EGCG), all-trans retinoic acid (ATRA) and arsenic trioxide (ATO), it is better to demonstrate the important potential role and mechanism of Pin1 in resistance and sensitization to cancer therapies. It will provide new therapeutic approaches for clinical reversal and prevention of tumor resistance by employing synergistic administration of Pin1 inhibitors and chemotherapeutics, implementing combination therapy of Pin1-related cancer signaling pathway inhibitors and Pin1 inhibitors, and exploiting novel Pin1-specific inhibitors. The development of tumor therapeutic resistance is one of the important reasons for the failure of antitumor therapy. Starting with multiple targets and multiple signaling pathways is helpful in understanding the mechanism of tumor resistance. The overexpression of prolyl isomerase Pin1 is highly correlated with the malignancy of cancer, since Pin1 controls many oncogenes and tumor suppressors, as well as a variety of cancer-driving signaling pathways. Strikingly, numerous studies have shown that Pin1 is directly involved in therapeutic resistance. In this review, we mainly summarize the functions and mechanisms of Pin1 in therapeutic resistance of multifarious cancers, such as breast, liver, and pancreatic carcinomas. Furtherly, from the perspective of Pin1-driven cancer signaling pathways including Raf/MEK/ERK, PI3K/Akt, Wnt/β-catenin, NF-κB, as well as Pin1 inhibitors containing juglone, epigallocatechin-3-gallate (EGCG), all-trans retinoic acid (ATRA) and arsenic trioxide (ATO), it is better to demonstrate the important potential role and mechanism of Pin1 in resistance and sensitization to cancer therapies. It will provide new therapeutic approaches for clinical reversal and prevention of tumor resistance by employing synergistic administration of Pin1 inhibitors and chemotherapeutics, implementing combination therapy of Pin1-related cancer signaling pathway inhibitors and Pin1 inhibitors, and exploiting novel Pin1-specific inhibitors. Ser/Thr-Pro Elsevier ALL Elsevier TAM Elsevier BCSCs Elsevier RKIP Elsevier PPIase Elsevier ADM Elsevier HIF-1α Elsevier UA Elsevier AP-1 Elsevier XPO5 Elsevier TNBC Elsevier CSCs Elsevier AML Elsevier BCRP Elsevier P-gp Elsevier TRAIL Elsevier EGCG Elsevier HCC Elsevier Tex10 Elsevier DOX Elsevier EMT Elsevier ER Elsevier AR Elsevier PDAC Elsevier CRC Elsevier EET Elsevier HNSCC Elsevier SMRT Elsevier ATRA Elsevier CRPC Elsevier HBx Elsevier FDA Elsevier VCR Elsevier EGFR Elsevier Hsp90 Elsevier IκB Elsevier CAFs Elsevier IRAK1 Elsevier TLR Elsevier TFAP2A Elsevier NSCLC Elsevier HIP1R Elsevier IKK Elsevier BIO Elsevier TME Elsevier PML Elsevier FAS Elsevier Pin1 Elsevier ATO Elsevier HER2 Elsevier APL Elsevier 5-FU Elsevier Xue, Xuezhen oth Chen, Yan oth Zheng, Ning oth Wang, Jichuang oth Enthalten in Academic Press Deng, Lixing ELSEVIER Social insurance premiums and corporate cash holdings: Evidence from social insurance law in China 2022 the official journal of the Italian Pharmacological Society London (DE-627)ELV008224951 volume:184 year:2022 pages:0 https://doi.org/10.1016/j.phrs.2022.106456 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U AR 184 2022 0 |
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Targeting prolyl isomerase Pin1 as a promising strategy to overcome resistance to cancer therapies |
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The development of tumor therapeutic resistance is one of the important reasons for the failure of antitumor therapy. Starting with multiple targets and multiple signaling pathways is helpful in understanding the mechanism of tumor resistance. The overexpression of prolyl isomerase Pin1 is highly correlated with the malignancy of cancer, since Pin1 controls many oncogenes and tumor suppressors, as well as a variety of cancer-driving signaling pathways. Strikingly, numerous studies have shown that Pin1 is directly involved in therapeutic resistance. In this review, we mainly summarize the functions and mechanisms of Pin1 in therapeutic resistance of multifarious cancers, such as breast, liver, and pancreatic carcinomas. Furtherly, from the perspective of Pin1-driven cancer signaling pathways including Raf/MEK/ERK, PI3K/Akt, Wnt/β-catenin, NF-κB, as well as Pin1 inhibitors containing juglone, epigallocatechin-3-gallate (EGCG), all-trans retinoic acid (ATRA) and arsenic trioxide (ATO), it is better to demonstrate the important potential role and mechanism of Pin1 in resistance and sensitization to cancer therapies. It will provide new therapeutic approaches for clinical reversal and prevention of tumor resistance by employing synergistic administration of Pin1 inhibitors and chemotherapeutics, implementing combination therapy of Pin1-related cancer signaling pathway inhibitors and Pin1 inhibitors, and exploiting novel Pin1-specific inhibitors. |
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The development of tumor therapeutic resistance is one of the important reasons for the failure of antitumor therapy. Starting with multiple targets and multiple signaling pathways is helpful in understanding the mechanism of tumor resistance. The overexpression of prolyl isomerase Pin1 is highly correlated with the malignancy of cancer, since Pin1 controls many oncogenes and tumor suppressors, as well as a variety of cancer-driving signaling pathways. Strikingly, numerous studies have shown that Pin1 is directly involved in therapeutic resistance. In this review, we mainly summarize the functions and mechanisms of Pin1 in therapeutic resistance of multifarious cancers, such as breast, liver, and pancreatic carcinomas. Furtherly, from the perspective of Pin1-driven cancer signaling pathways including Raf/MEK/ERK, PI3K/Akt, Wnt/β-catenin, NF-κB, as well as Pin1 inhibitors containing juglone, epigallocatechin-3-gallate (EGCG), all-trans retinoic acid (ATRA) and arsenic trioxide (ATO), it is better to demonstrate the important potential role and mechanism of Pin1 in resistance and sensitization to cancer therapies. It will provide new therapeutic approaches for clinical reversal and prevention of tumor resistance by employing synergistic administration of Pin1 inhibitors and chemotherapeutics, implementing combination therapy of Pin1-related cancer signaling pathway inhibitors and Pin1 inhibitors, and exploiting novel Pin1-specific inhibitors. |
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The development of tumor therapeutic resistance is one of the important reasons for the failure of antitumor therapy. Starting with multiple targets and multiple signaling pathways is helpful in understanding the mechanism of tumor resistance. The overexpression of prolyl isomerase Pin1 is highly correlated with the malignancy of cancer, since Pin1 controls many oncogenes and tumor suppressors, as well as a variety of cancer-driving signaling pathways. Strikingly, numerous studies have shown that Pin1 is directly involved in therapeutic resistance. In this review, we mainly summarize the functions and mechanisms of Pin1 in therapeutic resistance of multifarious cancers, such as breast, liver, and pancreatic carcinomas. Furtherly, from the perspective of Pin1-driven cancer signaling pathways including Raf/MEK/ERK, PI3K/Akt, Wnt/β-catenin, NF-κB, as well as Pin1 inhibitors containing juglone, epigallocatechin-3-gallate (EGCG), all-trans retinoic acid (ATRA) and arsenic trioxide (ATO), it is better to demonstrate the important potential role and mechanism of Pin1 in resistance and sensitization to cancer therapies. It will provide new therapeutic approaches for clinical reversal and prevention of tumor resistance by employing synergistic administration of Pin1 inhibitors and chemotherapeutics, implementing combination therapy of Pin1-related cancer signaling pathway inhibitors and Pin1 inhibitors, and exploiting novel Pin1-specific inhibitors. |
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<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">ELV059148152</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230626052321.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">221103s2022 xx |||||o 00| ||eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1016/j.phrs.2022.106456</subfield><subfield code="2">doi</subfield></datafield><datafield tag="028" ind1="5" ind2="2"><subfield code="a">/cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001925.pica</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)ELV059148152</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(ELSEVIER)S1043-6618(22)00402-9</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">330</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Wu, Wenda</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Targeting prolyl isomerase Pin1 as a promising strategy to overcome resistance to cancer therapies</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2022transfer abstract</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zzz</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">z</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zu</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">The development of tumor therapeutic resistance is one of the important reasons for the failure of antitumor therapy. Starting with multiple targets and multiple signaling pathways is helpful in understanding the mechanism of tumor resistance. The overexpression of prolyl isomerase Pin1 is highly correlated with the malignancy of cancer, since Pin1 controls many oncogenes and tumor suppressors, as well as a variety of cancer-driving signaling pathways. Strikingly, numerous studies have shown that Pin1 is directly involved in therapeutic resistance. In this review, we mainly summarize the functions and mechanisms of Pin1 in therapeutic resistance of multifarious cancers, such as breast, liver, and pancreatic carcinomas. Furtherly, from the perspective of Pin1-driven cancer signaling pathways including Raf/MEK/ERK, PI3K/Akt, Wnt/β-catenin, NF-κB, as well as Pin1 inhibitors containing juglone, epigallocatechin-3-gallate (EGCG), all-trans retinoic acid (ATRA) and arsenic trioxide (ATO), it is better to demonstrate the important potential role and mechanism of Pin1 in resistance and sensitization to cancer therapies. It will provide new therapeutic approaches for clinical reversal and prevention of tumor resistance by employing synergistic administration of Pin1 inhibitors and chemotherapeutics, implementing combination therapy of Pin1-related cancer signaling pathway inhibitors and Pin1 inhibitors, and exploiting novel Pin1-specific inhibitors.</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">The development of tumor therapeutic resistance is one of the important reasons for the failure of antitumor therapy. Starting with multiple targets and multiple signaling pathways is helpful in understanding the mechanism of tumor resistance. The overexpression of prolyl isomerase Pin1 is highly correlated with the malignancy of cancer, since Pin1 controls many oncogenes and tumor suppressors, as well as a variety of cancer-driving signaling pathways. Strikingly, numerous studies have shown that Pin1 is directly involved in therapeutic resistance. In this review, we mainly summarize the functions and mechanisms of Pin1 in therapeutic resistance of multifarious cancers, such as breast, liver, and pancreatic carcinomas. Furtherly, from the perspective of Pin1-driven cancer signaling pathways including Raf/MEK/ERK, PI3K/Akt, Wnt/β-catenin, NF-κB, as well as Pin1 inhibitors containing juglone, epigallocatechin-3-gallate (EGCG), all-trans retinoic acid (ATRA) and arsenic trioxide (ATO), it is better to demonstrate the important potential role and mechanism of Pin1 in resistance and sensitization to cancer therapies. 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