The Experts below are selected from a list of 5373 Experts worldwide ranked by ideXlab platform
Kuanghung Cheng - One of the best experts on this subject based on the ideXlab platform.
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stem cell marker Nestin is critical for tgf β1 mediated tumor progression in pancreatic cancer
Molecular Cancer Research, 2013Co-Authors: Hueiting Su, Chingchieh Weng, Pijung Hsiao, Lihua Chen, Yuwen Chen, Kuanghung ChengAbstract:The stem cell marker Nestin is an intermediate filament Protein that plays an important role in cell integrity, migration, and differentiation. Nestin expression occurs in approximately one third of pancreatic ductal adenocarcinoma (PDAC), and its expression strongly correlates with tumor staging and metastasis. Little is known about the mechanisms by which Nestin influences PDAC progression. Here, Nestin overexpression in PDAC cells increased cell motility and drove phenotypic changes associated with the epithelial-mesenchymal transition (EMT) in vitro; conversely, knockdown of endogenous Nestin expression reduced the migration rate and reverted cells to a more epithelial phenotype. Mouse xenograft studies showed that knockdown of Nestin significantly reduced tumor incidence and volume. Nestin Protein expression was associated with Smad4 status in PDAC cells; hence, Nestin expression might be regulated by the TGF-b1/Smad4 pathway in PDAC. We examined Nestin expression after TGF-b1 treatment in human pancreatic cancer PANC-1 and PANC-1 shSmad4 cells. The TGF-b1/Smad4 pathway induced Nestin Protein expression in PDAC cells in a Smad4dependent manner. Moreover, increased Nestin expression caused a positive feedback regulator of the TGF-b1 signaling system. In addition, hypoxia was shown to induce Nestin expression in PDAC cells, and the hypoxiainduced expression of Nestin is mediated by the TGF-b1/Smad4 pathway. Finally, the antimicrotubule inhibitors, cytochalasin D and withaferin A, exhibited anti-Nestin activity; these inhibitors might be potential antimetastatic drugs. Our findings uncovered a novel role of Nestin in regulating TGF-b1-induced EMT. AntiNestin therapeutics may serve as a potential treatment for PDAC metastasis. Mol Cancer Res; 11(7); 768–79. � 2013 AACR.
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stem cell marker Nestin is critical for tgf β1 mediated tumor progression in pancreatic cancer
Molecular Cancer Research, 2013Co-Authors: Chingchieh Weng, Pijung Hsiao, Lihua Chen, Yuwen Chen, Tzulei Kuo, Kungkai Kuo, Kuanghung ChengAbstract:The stem cell marker Nestin is an intermediate filament Protein that plays an important role in cell integrity, migration, and differentiation. Nestin expression occurs in approximately one third of pancreatic ductal adenocarcinoma (PDAC), and its expression strongly correlates with tumor staging and metastasis. Little is known about the mechanisms by which Nestin influences PDAC progression. Here, Nestin overexpression in PDAC cells increased cell motility and drove phenotypic changes associated with the epithelial-mesenchymal transition (EMT) in vitro; conversely, knockdown of endogenous Nestin expression reduced the migration rate and reverted cells to a more epithelial phenotype. Mouse xenograft studies showed that knockdown of Nestin significantly reduced tumor incidence and volume. Nestin Protein expression was associated with Smad4 status in PDAC cells; hence, Nestin expression might be regulated by the TGF-β1/Smad4 pathway in PDAC. We examined Nestin expression after TGF-β1 treatment in human pancreatic cancer PANC-1 and PANC-1 shSmad4 cells. The TGF-β1/Smad4 pathway induced Nestin Protein expression in PDAC cells in a Smad4-dependent manner. Moreover, increased Nestin expression caused a positive feedback regulator of the TGF-β1 signaling system. In addition, hypoxia was shown to induce Nestin expression in PDAC cells, and the hypoxia-induced expression of Nestin is mediated by the TGF-β1/Smad4 pathway. Finally, the antimicrotubule inhibitors, cytochalasin D and withaferin A, exhibited anti-Nestin activity; these inhibitors might be potential antimetastatic drugs. Our findings uncovered a novel role of Nestin in regulating TGF-β1-induced EMT. Anti-Nestin therapeutics may serve as a potential treatment for PDAC metastasis.
Chingchieh Weng - One of the best experts on this subject based on the ideXlab platform.
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stem cell marker Nestin is critical for tgf β1 mediated tumor progression in pancreatic cancer
Molecular Cancer Research, 2013Co-Authors: Hueiting Su, Chingchieh Weng, Pijung Hsiao, Lihua Chen, Yuwen Chen, Kuanghung ChengAbstract:The stem cell marker Nestin is an intermediate filament Protein that plays an important role in cell integrity, migration, and differentiation. Nestin expression occurs in approximately one third of pancreatic ductal adenocarcinoma (PDAC), and its expression strongly correlates with tumor staging and metastasis. Little is known about the mechanisms by which Nestin influences PDAC progression. Here, Nestin overexpression in PDAC cells increased cell motility and drove phenotypic changes associated with the epithelial-mesenchymal transition (EMT) in vitro; conversely, knockdown of endogenous Nestin expression reduced the migration rate and reverted cells to a more epithelial phenotype. Mouse xenograft studies showed that knockdown of Nestin significantly reduced tumor incidence and volume. Nestin Protein expression was associated with Smad4 status in PDAC cells; hence, Nestin expression might be regulated by the TGF-b1/Smad4 pathway in PDAC. We examined Nestin expression after TGF-b1 treatment in human pancreatic cancer PANC-1 and PANC-1 shSmad4 cells. The TGF-b1/Smad4 pathway induced Nestin Protein expression in PDAC cells in a Smad4dependent manner. Moreover, increased Nestin expression caused a positive feedback regulator of the TGF-b1 signaling system. In addition, hypoxia was shown to induce Nestin expression in PDAC cells, and the hypoxiainduced expression of Nestin is mediated by the TGF-b1/Smad4 pathway. Finally, the antimicrotubule inhibitors, cytochalasin D and withaferin A, exhibited anti-Nestin activity; these inhibitors might be potential antimetastatic drugs. Our findings uncovered a novel role of Nestin in regulating TGF-b1-induced EMT. AntiNestin therapeutics may serve as a potential treatment for PDAC metastasis. Mol Cancer Res; 11(7); 768–79. � 2013 AACR.
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stem cell marker Nestin is critical for tgf β1 mediated tumor progression in pancreatic cancer
Molecular Cancer Research, 2013Co-Authors: Chingchieh Weng, Pijung Hsiao, Lihua Chen, Yuwen Chen, Tzulei Kuo, Kungkai Kuo, Kuanghung ChengAbstract:The stem cell marker Nestin is an intermediate filament Protein that plays an important role in cell integrity, migration, and differentiation. Nestin expression occurs in approximately one third of pancreatic ductal adenocarcinoma (PDAC), and its expression strongly correlates with tumor staging and metastasis. Little is known about the mechanisms by which Nestin influences PDAC progression. Here, Nestin overexpression in PDAC cells increased cell motility and drove phenotypic changes associated with the epithelial-mesenchymal transition (EMT) in vitro; conversely, knockdown of endogenous Nestin expression reduced the migration rate and reverted cells to a more epithelial phenotype. Mouse xenograft studies showed that knockdown of Nestin significantly reduced tumor incidence and volume. Nestin Protein expression was associated with Smad4 status in PDAC cells; hence, Nestin expression might be regulated by the TGF-β1/Smad4 pathway in PDAC. We examined Nestin expression after TGF-β1 treatment in human pancreatic cancer PANC-1 and PANC-1 shSmad4 cells. The TGF-β1/Smad4 pathway induced Nestin Protein expression in PDAC cells in a Smad4-dependent manner. Moreover, increased Nestin expression caused a positive feedback regulator of the TGF-β1 signaling system. In addition, hypoxia was shown to induce Nestin expression in PDAC cells, and the hypoxia-induced expression of Nestin is mediated by the TGF-β1/Smad4 pathway. Finally, the antimicrotubule inhibitors, cytochalasin D and withaferin A, exhibited anti-Nestin activity; these inhibitors might be potential antimetastatic drugs. Our findings uncovered a novel role of Nestin in regulating TGF-β1-induced EMT. Anti-Nestin therapeutics may serve as a potential treatment for PDAC metastasis.
Yuwen Chen - One of the best experts on this subject based on the ideXlab platform.
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stem cell marker Nestin is critical for tgf β1 mediated tumor progression in pancreatic cancer
Molecular Cancer Research, 2013Co-Authors: Hueiting Su, Chingchieh Weng, Pijung Hsiao, Lihua Chen, Yuwen Chen, Kuanghung ChengAbstract:The stem cell marker Nestin is an intermediate filament Protein that plays an important role in cell integrity, migration, and differentiation. Nestin expression occurs in approximately one third of pancreatic ductal adenocarcinoma (PDAC), and its expression strongly correlates with tumor staging and metastasis. Little is known about the mechanisms by which Nestin influences PDAC progression. Here, Nestin overexpression in PDAC cells increased cell motility and drove phenotypic changes associated with the epithelial-mesenchymal transition (EMT) in vitro; conversely, knockdown of endogenous Nestin expression reduced the migration rate and reverted cells to a more epithelial phenotype. Mouse xenograft studies showed that knockdown of Nestin significantly reduced tumor incidence and volume. Nestin Protein expression was associated with Smad4 status in PDAC cells; hence, Nestin expression might be regulated by the TGF-b1/Smad4 pathway in PDAC. We examined Nestin expression after TGF-b1 treatment in human pancreatic cancer PANC-1 and PANC-1 shSmad4 cells. The TGF-b1/Smad4 pathway induced Nestin Protein expression in PDAC cells in a Smad4dependent manner. Moreover, increased Nestin expression caused a positive feedback regulator of the TGF-b1 signaling system. In addition, hypoxia was shown to induce Nestin expression in PDAC cells, and the hypoxiainduced expression of Nestin is mediated by the TGF-b1/Smad4 pathway. Finally, the antimicrotubule inhibitors, cytochalasin D and withaferin A, exhibited anti-Nestin activity; these inhibitors might be potential antimetastatic drugs. Our findings uncovered a novel role of Nestin in regulating TGF-b1-induced EMT. AntiNestin therapeutics may serve as a potential treatment for PDAC metastasis. Mol Cancer Res; 11(7); 768–79. � 2013 AACR.
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stem cell marker Nestin is critical for tgf β1 mediated tumor progression in pancreatic cancer
Molecular Cancer Research, 2013Co-Authors: Chingchieh Weng, Pijung Hsiao, Lihua Chen, Yuwen Chen, Tzulei Kuo, Kungkai Kuo, Kuanghung ChengAbstract:The stem cell marker Nestin is an intermediate filament Protein that plays an important role in cell integrity, migration, and differentiation. Nestin expression occurs in approximately one third of pancreatic ductal adenocarcinoma (PDAC), and its expression strongly correlates with tumor staging and metastasis. Little is known about the mechanisms by which Nestin influences PDAC progression. Here, Nestin overexpression in PDAC cells increased cell motility and drove phenotypic changes associated with the epithelial-mesenchymal transition (EMT) in vitro; conversely, knockdown of endogenous Nestin expression reduced the migration rate and reverted cells to a more epithelial phenotype. Mouse xenograft studies showed that knockdown of Nestin significantly reduced tumor incidence and volume. Nestin Protein expression was associated with Smad4 status in PDAC cells; hence, Nestin expression might be regulated by the TGF-β1/Smad4 pathway in PDAC. We examined Nestin expression after TGF-β1 treatment in human pancreatic cancer PANC-1 and PANC-1 shSmad4 cells. The TGF-β1/Smad4 pathway induced Nestin Protein expression in PDAC cells in a Smad4-dependent manner. Moreover, increased Nestin expression caused a positive feedback regulator of the TGF-β1 signaling system. In addition, hypoxia was shown to induce Nestin expression in PDAC cells, and the hypoxia-induced expression of Nestin is mediated by the TGF-β1/Smad4 pathway. Finally, the antimicrotubule inhibitors, cytochalasin D and withaferin A, exhibited anti-Nestin activity; these inhibitors might be potential antimetastatic drugs. Our findings uncovered a novel role of Nestin in regulating TGF-β1-induced EMT. Anti-Nestin therapeutics may serve as a potential treatment for PDAC metastasis.
Pijung Hsiao - One of the best experts on this subject based on the ideXlab platform.
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stem cell marker Nestin is critical for tgf β1 mediated tumor progression in pancreatic cancer
Molecular Cancer Research, 2013Co-Authors: Hueiting Su, Chingchieh Weng, Pijung Hsiao, Lihua Chen, Yuwen Chen, Kuanghung ChengAbstract:The stem cell marker Nestin is an intermediate filament Protein that plays an important role in cell integrity, migration, and differentiation. Nestin expression occurs in approximately one third of pancreatic ductal adenocarcinoma (PDAC), and its expression strongly correlates with tumor staging and metastasis. Little is known about the mechanisms by which Nestin influences PDAC progression. Here, Nestin overexpression in PDAC cells increased cell motility and drove phenotypic changes associated with the epithelial-mesenchymal transition (EMT) in vitro; conversely, knockdown of endogenous Nestin expression reduced the migration rate and reverted cells to a more epithelial phenotype. Mouse xenograft studies showed that knockdown of Nestin significantly reduced tumor incidence and volume. Nestin Protein expression was associated with Smad4 status in PDAC cells; hence, Nestin expression might be regulated by the TGF-b1/Smad4 pathway in PDAC. We examined Nestin expression after TGF-b1 treatment in human pancreatic cancer PANC-1 and PANC-1 shSmad4 cells. The TGF-b1/Smad4 pathway induced Nestin Protein expression in PDAC cells in a Smad4dependent manner. Moreover, increased Nestin expression caused a positive feedback regulator of the TGF-b1 signaling system. In addition, hypoxia was shown to induce Nestin expression in PDAC cells, and the hypoxiainduced expression of Nestin is mediated by the TGF-b1/Smad4 pathway. Finally, the antimicrotubule inhibitors, cytochalasin D and withaferin A, exhibited anti-Nestin activity; these inhibitors might be potential antimetastatic drugs. Our findings uncovered a novel role of Nestin in regulating TGF-b1-induced EMT. AntiNestin therapeutics may serve as a potential treatment for PDAC metastasis. Mol Cancer Res; 11(7); 768–79. � 2013 AACR.
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stem cell marker Nestin is critical for tgf β1 mediated tumor progression in pancreatic cancer
Molecular Cancer Research, 2013Co-Authors: Chingchieh Weng, Pijung Hsiao, Lihua Chen, Yuwen Chen, Tzulei Kuo, Kungkai Kuo, Kuanghung ChengAbstract:The stem cell marker Nestin is an intermediate filament Protein that plays an important role in cell integrity, migration, and differentiation. Nestin expression occurs in approximately one third of pancreatic ductal adenocarcinoma (PDAC), and its expression strongly correlates with tumor staging and metastasis. Little is known about the mechanisms by which Nestin influences PDAC progression. Here, Nestin overexpression in PDAC cells increased cell motility and drove phenotypic changes associated with the epithelial-mesenchymal transition (EMT) in vitro; conversely, knockdown of endogenous Nestin expression reduced the migration rate and reverted cells to a more epithelial phenotype. Mouse xenograft studies showed that knockdown of Nestin significantly reduced tumor incidence and volume. Nestin Protein expression was associated with Smad4 status in PDAC cells; hence, Nestin expression might be regulated by the TGF-β1/Smad4 pathway in PDAC. We examined Nestin expression after TGF-β1 treatment in human pancreatic cancer PANC-1 and PANC-1 shSmad4 cells. The TGF-β1/Smad4 pathway induced Nestin Protein expression in PDAC cells in a Smad4-dependent manner. Moreover, increased Nestin expression caused a positive feedback regulator of the TGF-β1 signaling system. In addition, hypoxia was shown to induce Nestin expression in PDAC cells, and the hypoxia-induced expression of Nestin is mediated by the TGF-β1/Smad4 pathway. Finally, the antimicrotubule inhibitors, cytochalasin D and withaferin A, exhibited anti-Nestin activity; these inhibitors might be potential antimetastatic drugs. Our findings uncovered a novel role of Nestin in regulating TGF-β1-induced EMT. Anti-Nestin therapeutics may serve as a potential treatment for PDAC metastasis.
Lihua Chen - One of the best experts on this subject based on the ideXlab platform.
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stem cell marker Nestin is critical for tgf β1 mediated tumor progression in pancreatic cancer
Molecular Cancer Research, 2013Co-Authors: Hueiting Su, Chingchieh Weng, Pijung Hsiao, Lihua Chen, Yuwen Chen, Kuanghung ChengAbstract:The stem cell marker Nestin is an intermediate filament Protein that plays an important role in cell integrity, migration, and differentiation. Nestin expression occurs in approximately one third of pancreatic ductal adenocarcinoma (PDAC), and its expression strongly correlates with tumor staging and metastasis. Little is known about the mechanisms by which Nestin influences PDAC progression. Here, Nestin overexpression in PDAC cells increased cell motility and drove phenotypic changes associated with the epithelial-mesenchymal transition (EMT) in vitro; conversely, knockdown of endogenous Nestin expression reduced the migration rate and reverted cells to a more epithelial phenotype. Mouse xenograft studies showed that knockdown of Nestin significantly reduced tumor incidence and volume. Nestin Protein expression was associated with Smad4 status in PDAC cells; hence, Nestin expression might be regulated by the TGF-b1/Smad4 pathway in PDAC. We examined Nestin expression after TGF-b1 treatment in human pancreatic cancer PANC-1 and PANC-1 shSmad4 cells. The TGF-b1/Smad4 pathway induced Nestin Protein expression in PDAC cells in a Smad4dependent manner. Moreover, increased Nestin expression caused a positive feedback regulator of the TGF-b1 signaling system. In addition, hypoxia was shown to induce Nestin expression in PDAC cells, and the hypoxiainduced expression of Nestin is mediated by the TGF-b1/Smad4 pathway. Finally, the antimicrotubule inhibitors, cytochalasin D and withaferin A, exhibited anti-Nestin activity; these inhibitors might be potential antimetastatic drugs. Our findings uncovered a novel role of Nestin in regulating TGF-b1-induced EMT. AntiNestin therapeutics may serve as a potential treatment for PDAC metastasis. Mol Cancer Res; 11(7); 768–79. � 2013 AACR.
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stem cell marker Nestin is critical for tgf β1 mediated tumor progression in pancreatic cancer
Molecular Cancer Research, 2013Co-Authors: Chingchieh Weng, Pijung Hsiao, Lihua Chen, Yuwen Chen, Tzulei Kuo, Kungkai Kuo, Kuanghung ChengAbstract:The stem cell marker Nestin is an intermediate filament Protein that plays an important role in cell integrity, migration, and differentiation. Nestin expression occurs in approximately one third of pancreatic ductal adenocarcinoma (PDAC), and its expression strongly correlates with tumor staging and metastasis. Little is known about the mechanisms by which Nestin influences PDAC progression. Here, Nestin overexpression in PDAC cells increased cell motility and drove phenotypic changes associated with the epithelial-mesenchymal transition (EMT) in vitro; conversely, knockdown of endogenous Nestin expression reduced the migration rate and reverted cells to a more epithelial phenotype. Mouse xenograft studies showed that knockdown of Nestin significantly reduced tumor incidence and volume. Nestin Protein expression was associated with Smad4 status in PDAC cells; hence, Nestin expression might be regulated by the TGF-β1/Smad4 pathway in PDAC. We examined Nestin expression after TGF-β1 treatment in human pancreatic cancer PANC-1 and PANC-1 shSmad4 cells. The TGF-β1/Smad4 pathway induced Nestin Protein expression in PDAC cells in a Smad4-dependent manner. Moreover, increased Nestin expression caused a positive feedback regulator of the TGF-β1 signaling system. In addition, hypoxia was shown to induce Nestin expression in PDAC cells, and the hypoxia-induced expression of Nestin is mediated by the TGF-β1/Smad4 pathway. Finally, the antimicrotubule inhibitors, cytochalasin D and withaferin A, exhibited anti-Nestin activity; these inhibitors might be potential antimetastatic drugs. Our findings uncovered a novel role of Nestin in regulating TGF-β1-induced EMT. Anti-Nestin therapeutics may serve as a potential treatment for PDAC metastasis.
