The Experts below are selected from a list of 189 Experts worldwide ranked by ideXlab platform
Hsi-wen Yeh - One of the best experts on this subject based on the ideXlab platform.
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PSPC1 mediates TGF-β1 Autocrine Signalling and Smad2/3 target switching to promote EMT, stemness and metastasis.
Nature cell biology, 2018Co-Authors: Hsi-wen Yeh, En-chi Hsu, Szu-shuo Lee, Yaw-dong Lang, Yuh-charn Lin, Chieh-yu Chang, Suz-yi Lee, Jou-ho ShihAbstract:Activation of metastatic reprogramming is critical for tumour metastasis. However, more detailed knowledge of the underlying mechanism is needed to enable targeted intervention. Here, we show that paraspeckle component 1 (PSPC1), identified in an aberrant 13q12.11 locus, is upregulated and associated with poor survival in patients with cancer. PSPC1 promotes tumorigenesis, epithelial-to-mesenchymal transition (EMT), stemness and metastasis in multiple cell types and in spontaneous mouse cancer models. PSPC1 is the master activator for transcription factors of EMT and stemness and accompanies c-Myc activation to facilitate tumour growth. PSPC1 increases transforming growth factor-β1 (TGF-β1) secretion through an interaction with phosphorylated and nuclear Smad2/3 to potentiate TGF-β1 Autocrine Signalling. Moreover, PSPC1 acts as a contextual determinant of the TGF-β1 pro-metastatic switch to alter Smad2/3 binding preference from tumour-suppressor to pro-metastatic genes. Having validated the PSPC1-Smads-TGF-β1 axis in various cancers, we conclude that PSPC1 is a master activator of pro-metastatic switches and a potential target for anti-metastasis drugs.
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pspc1 mediates tgf β1 Autocrine Signalling and smad2 3 target switching to promote emt stemness and metastasis
Nature Cell Biology, 2018Co-Authors: Hsi-wen Yeh, En-chi Hsu, Szu-shuo Lee, Yaw-dong Lang, Yuh-charn Lin, Chieh-yu Chang, Suz-yi LeeAbstract:Activation of metastatic reprogramming is critical for tumour metastasis. However, more detailed knowledge of the underlying mechanism is needed to enable targeted intervention. Here, we show that paraspeckle component 1 (PSPC1), identified in an aberrant 13q12.11 locus, is upregulated and associated with poor survival in patients with cancer. PSPC1 promotes tumorigenesis, epithelial-to-mesenchymal transition (EMT), stemness and metastasis in multiple cell types and in spontaneous mouse cancer models. PSPC1 is the master activator for transcription factors of EMT and stemness and accompanies c-Myc activation to facilitate tumour growth. PSPC1 increases transforming growth factor-β1 (TGF-β1) secretion through an interaction with phosphorylated and nuclear Smad2/3 to potentiate TGF-β1 Autocrine Signalling. Moreover, PSPC1 acts as a contextual determinant of the TGF-β1 pro-metastatic switch to alter Smad2/3 binding preference from tumour-suppressor to pro-metastatic genes. Having validated the PSPC1-Smads-TGF-β1 axis in various cancers, we conclude that PSPC1 is a master activator of pro-metastatic switches and a potential target for anti-metastasis drugs.
Suz-yi Lee - One of the best experts on this subject based on the ideXlab platform.
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PSPC1 mediates TGF-β1 Autocrine Signalling and Smad2/3 target switching to promote EMT, stemness and metastasis.
Nature cell biology, 2018Co-Authors: Hsi-wen Yeh, En-chi Hsu, Szu-shuo Lee, Yaw-dong Lang, Yuh-charn Lin, Chieh-yu Chang, Suz-yi Lee, Jou-ho ShihAbstract:Activation of metastatic reprogramming is critical for tumour metastasis. However, more detailed knowledge of the underlying mechanism is needed to enable targeted intervention. Here, we show that paraspeckle component 1 (PSPC1), identified in an aberrant 13q12.11 locus, is upregulated and associated with poor survival in patients with cancer. PSPC1 promotes tumorigenesis, epithelial-to-mesenchymal transition (EMT), stemness and metastasis in multiple cell types and in spontaneous mouse cancer models. PSPC1 is the master activator for transcription factors of EMT and stemness and accompanies c-Myc activation to facilitate tumour growth. PSPC1 increases transforming growth factor-β1 (TGF-β1) secretion through an interaction with phosphorylated and nuclear Smad2/3 to potentiate TGF-β1 Autocrine Signalling. Moreover, PSPC1 acts as a contextual determinant of the TGF-β1 pro-metastatic switch to alter Smad2/3 binding preference from tumour-suppressor to pro-metastatic genes. Having validated the PSPC1-Smads-TGF-β1 axis in various cancers, we conclude that PSPC1 is a master activator of pro-metastatic switches and a potential target for anti-metastasis drugs.
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pspc1 mediates tgf β1 Autocrine Signalling and smad2 3 target switching to promote emt stemness and metastasis
Nature Cell Biology, 2018Co-Authors: Hsi-wen Yeh, En-chi Hsu, Szu-shuo Lee, Yaw-dong Lang, Yuh-charn Lin, Chieh-yu Chang, Suz-yi LeeAbstract:Activation of metastatic reprogramming is critical for tumour metastasis. However, more detailed knowledge of the underlying mechanism is needed to enable targeted intervention. Here, we show that paraspeckle component 1 (PSPC1), identified in an aberrant 13q12.11 locus, is upregulated and associated with poor survival in patients with cancer. PSPC1 promotes tumorigenesis, epithelial-to-mesenchymal transition (EMT), stemness and metastasis in multiple cell types and in spontaneous mouse cancer models. PSPC1 is the master activator for transcription factors of EMT and stemness and accompanies c-Myc activation to facilitate tumour growth. PSPC1 increases transforming growth factor-β1 (TGF-β1) secretion through an interaction with phosphorylated and nuclear Smad2/3 to potentiate TGF-β1 Autocrine Signalling. Moreover, PSPC1 acts as a contextual determinant of the TGF-β1 pro-metastatic switch to alter Smad2/3 binding preference from tumour-suppressor to pro-metastatic genes. Having validated the PSPC1-Smads-TGF-β1 axis in various cancers, we conclude that PSPC1 is a master activator of pro-metastatic switches and a potential target for anti-metastasis drugs.
Chieh-yu Chang - One of the best experts on this subject based on the ideXlab platform.
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PSPC1 mediates TGF-β1 Autocrine Signalling and Smad2/3 target switching to promote EMT, stemness and metastasis.
Nature cell biology, 2018Co-Authors: Hsi-wen Yeh, En-chi Hsu, Szu-shuo Lee, Yaw-dong Lang, Yuh-charn Lin, Chieh-yu Chang, Suz-yi Lee, Jou-ho ShihAbstract:Activation of metastatic reprogramming is critical for tumour metastasis. However, more detailed knowledge of the underlying mechanism is needed to enable targeted intervention. Here, we show that paraspeckle component 1 (PSPC1), identified in an aberrant 13q12.11 locus, is upregulated and associated with poor survival in patients with cancer. PSPC1 promotes tumorigenesis, epithelial-to-mesenchymal transition (EMT), stemness and metastasis in multiple cell types and in spontaneous mouse cancer models. PSPC1 is the master activator for transcription factors of EMT and stemness and accompanies c-Myc activation to facilitate tumour growth. PSPC1 increases transforming growth factor-β1 (TGF-β1) secretion through an interaction with phosphorylated and nuclear Smad2/3 to potentiate TGF-β1 Autocrine Signalling. Moreover, PSPC1 acts as a contextual determinant of the TGF-β1 pro-metastatic switch to alter Smad2/3 binding preference from tumour-suppressor to pro-metastatic genes. Having validated the PSPC1-Smads-TGF-β1 axis in various cancers, we conclude that PSPC1 is a master activator of pro-metastatic switches and a potential target for anti-metastasis drugs.
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pspc1 mediates tgf β1 Autocrine Signalling and smad2 3 target switching to promote emt stemness and metastasis
Nature Cell Biology, 2018Co-Authors: Hsi-wen Yeh, En-chi Hsu, Szu-shuo Lee, Yaw-dong Lang, Yuh-charn Lin, Chieh-yu Chang, Suz-yi LeeAbstract:Activation of metastatic reprogramming is critical for tumour metastasis. However, more detailed knowledge of the underlying mechanism is needed to enable targeted intervention. Here, we show that paraspeckle component 1 (PSPC1), identified in an aberrant 13q12.11 locus, is upregulated and associated with poor survival in patients with cancer. PSPC1 promotes tumorigenesis, epithelial-to-mesenchymal transition (EMT), stemness and metastasis in multiple cell types and in spontaneous mouse cancer models. PSPC1 is the master activator for transcription factors of EMT and stemness and accompanies c-Myc activation to facilitate tumour growth. PSPC1 increases transforming growth factor-β1 (TGF-β1) secretion through an interaction with phosphorylated and nuclear Smad2/3 to potentiate TGF-β1 Autocrine Signalling. Moreover, PSPC1 acts as a contextual determinant of the TGF-β1 pro-metastatic switch to alter Smad2/3 binding preference from tumour-suppressor to pro-metastatic genes. Having validated the PSPC1-Smads-TGF-β1 axis in various cancers, we conclude that PSPC1 is a master activator of pro-metastatic switches and a potential target for anti-metastasis drugs.
Szu-shuo Lee - One of the best experts on this subject based on the ideXlab platform.
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PSPC1 mediates TGF-β1 Autocrine Signalling and Smad2/3 target switching to promote EMT, stemness and metastasis.
Nature cell biology, 2018Co-Authors: Hsi-wen Yeh, En-chi Hsu, Szu-shuo Lee, Yaw-dong Lang, Yuh-charn Lin, Chieh-yu Chang, Suz-yi Lee, Jou-ho ShihAbstract:Activation of metastatic reprogramming is critical for tumour metastasis. However, more detailed knowledge of the underlying mechanism is needed to enable targeted intervention. Here, we show that paraspeckle component 1 (PSPC1), identified in an aberrant 13q12.11 locus, is upregulated and associated with poor survival in patients with cancer. PSPC1 promotes tumorigenesis, epithelial-to-mesenchymal transition (EMT), stemness and metastasis in multiple cell types and in spontaneous mouse cancer models. PSPC1 is the master activator for transcription factors of EMT and stemness and accompanies c-Myc activation to facilitate tumour growth. PSPC1 increases transforming growth factor-β1 (TGF-β1) secretion through an interaction with phosphorylated and nuclear Smad2/3 to potentiate TGF-β1 Autocrine Signalling. Moreover, PSPC1 acts as a contextual determinant of the TGF-β1 pro-metastatic switch to alter Smad2/3 binding preference from tumour-suppressor to pro-metastatic genes. Having validated the PSPC1-Smads-TGF-β1 axis in various cancers, we conclude that PSPC1 is a master activator of pro-metastatic switches and a potential target for anti-metastasis drugs.
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pspc1 mediates tgf β1 Autocrine Signalling and smad2 3 target switching to promote emt stemness and metastasis
Nature Cell Biology, 2018Co-Authors: Hsi-wen Yeh, En-chi Hsu, Szu-shuo Lee, Yaw-dong Lang, Yuh-charn Lin, Chieh-yu Chang, Suz-yi LeeAbstract:Activation of metastatic reprogramming is critical for tumour metastasis. However, more detailed knowledge of the underlying mechanism is needed to enable targeted intervention. Here, we show that paraspeckle component 1 (PSPC1), identified in an aberrant 13q12.11 locus, is upregulated and associated with poor survival in patients with cancer. PSPC1 promotes tumorigenesis, epithelial-to-mesenchymal transition (EMT), stemness and metastasis in multiple cell types and in spontaneous mouse cancer models. PSPC1 is the master activator for transcription factors of EMT and stemness and accompanies c-Myc activation to facilitate tumour growth. PSPC1 increases transforming growth factor-β1 (TGF-β1) secretion through an interaction with phosphorylated and nuclear Smad2/3 to potentiate TGF-β1 Autocrine Signalling. Moreover, PSPC1 acts as a contextual determinant of the TGF-β1 pro-metastatic switch to alter Smad2/3 binding preference from tumour-suppressor to pro-metastatic genes. Having validated the PSPC1-Smads-TGF-β1 axis in various cancers, we conclude that PSPC1 is a master activator of pro-metastatic switches and a potential target for anti-metastasis drugs.
Robert Gniadecki - One of the best experts on this subject based on the ideXlab platform.
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the Autocrine tnfα Signalling loop in keratinocytes requires atypical pkc species and nf κb activation but is independent of cholesterol enriched membrane microdomains
Biochemical Pharmacology, 2007Co-Authors: Steen Lisby, Annesofie Faurschou, Robert GniadeckiAbstract:Abstract Tumor necrosis factor α (TNFα) is involved in the pathogenesis of many inflammatory skin diseases. Epidermal keratinocytes produce and respond to TNFα via the cognate type 1 receptor (TNFR1). Little is known about regulation of TNFα Signalling in this cell type. In this study, we report that in keratinocytes TNFα upregulates its own mRNA synthesis in an Autocrine manner. This response peaks at approximately 1 h of stimulation with TNFα but sustained elevated levels of TNFα mRNA are observed for up to 24 h after stimulation and are dependent on the presence of the soluble cytokine. This Autocrine response is mediated by the Signalling cascade comprising TNFR1, atypical protein kinase C (aPKC) species and the transcription factor NF-κB, but is not dependent on the integrity of cholesterol-enriched membrane microdomains (lipid rafts). TNFα-stimulated keratinocytes produced the membrane-bound form of TNFα. It is conceivable that the described Autocrine Signalling loop contributes to the proinflammatory TNFα effect in the skin. The discovery of the crucial roles of aPKC and NF-κB might have consequences for the development of more selective anti-TNFα therapies for inflammatory skin diseases.
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the Autocrine tnfα Signalling loop in keratinocytes requires atypical pkc species and nf κb activation but is independent of cholesterol enriched membrane microdomains
Biochemical Pharmacology, 2007Co-Authors: Steen Lisby, Annesofie Faurschou, Robert GniadeckiAbstract:Tumor necrosis factor alpha (TNFalpha) is involved in the pathogenesis of many inflammatory skin diseases. Epidermal keratinocytes produce and respond to TNFalpha via the cognate type 1 receptor (TNFR1). Little is known about regulation of TNFalpha Signalling in this cell type. In this study, we report that in keratinocytes TNFalpha upregulates its own mRNA synthesis in an Autocrine manner. This response peaks at approximately 1h of stimulation with TNFalpha but sustained elevated levels of TNFalpha mRNA are observed for up to 24h after stimulation and are dependent on the presence of the soluble cytokine. This Autocrine response is mediated by the Signalling cascade comprising TNFR1, atypical protein kinase C (aPKC) species and the transcription factor NF-kappaB, but is not dependent on the integrity of cholesterol-enriched membrane microdomains (lipid rafts). TNFalpha-stimulated keratinocytes produced the membrane-bound form of TNFalpha. It is conceivable that the described Autocrine Signalling loop contributes to the proinflammatory TNFalpha effect in the skin. The discovery of the crucial roles of aPKC and NF-kappaB might have consequences for the development of more selective anti-TNFalpha therapies for inflammatory skin diseases.
