We are analyzing https://link.springer.com/article/10.1186/s13046-019-1088-0.

Title:
LRG-1 promotes pancreatic cancer growth and metastasis via modulation of the EGFR/p38 signaling | Journal of Experimental & Clinical Cancer Research
Description:
Background The abnormal expression of leucine-rich-alpha-2-glycoprotein 1 (LRG-1) is reported to be associated with multiple malignancies, but its role in the progression of pancreatic ductal adenocarcinoma (PDAC) remains to be determined. Methods The expression of LRG-1 was assessed in PDAC tissues by RT-PCR, Western blot and immunohistochemistry. LRG-1-silenced or overexpressed cell lines were constructed using shRNA or LRG-1-overexpressing plasmids. EdU incorporation assay, Transwell invasion and wound-healing assays were performed to evaluate the proliferation, invasion and migration of PDAC cells. In addition, protein expression of the mitogen-activated protein kinase (MAPK) pathway was detected using Western blot. Finally, Co-immunoprecipitation assay was conducted in search of the potential interaction between LRG-1 and epidermal growth factor receptor (EGFR). Results The expression of LRG-1 in PDAC tissue was significantly higher than that in adjacent normal tissue, and high LRG-1 expression predicted poor survival and a late tumor stage. In addition, LRG-1 markedly promoted the viability, proliferation, migration and invasion of PDAC cells in vitro and facilitated tumor growth in vivo. More importantly, we revealed that these bioactivities of LRG-1 might result from its selective interaction with EGFR, which might further activate the p38/MAPK signaling pathways. Conclusion LRG-1 may prove to be a promising biomarker for predicting prognosis of PDAC patients. Inhibition of LRG-1 or its downstream pathway could be a potential therapeutic target for the treatment of PDAC.
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Keywords {🔍}

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Topics {✒️}

egfr/p38-mapk/sp1-dependent signalling integrin/egfr-erk/mapk signaling pathway leucine-rich-alpha-2-glycoprotein-1 mapk de-liang fu mitogen-activated protein kinase leucine-rich-alpha-2-glycoprotein 1 leucine-rich alpha-2-glycoprotein-1 leucine-rich-alpha-2-glycoprotein-1 leucine-rich alpha-2 glycoprotein tgf-β accessory receptor regulating igf-1/igf-1r signaling tgf-beta signaling pathway article download pdf leucine-rich alpha2-glycoprotein-1 pro shun-xing zhang pancreatic ductal adenocarcinoma epidermal growth factor p38/mapk signaling pathway apc-interacting protein mapre1 tumor necrosis factor-α p38/mapk signaling pathways early-stage pancreatic cancer fibroblast growth factor m-mlv reverse transcriptase lrg-1-induced p38 phosphorylation egfr/p38 signalling activation igf-1-mediated pi3k/akt fucoidan/fgf-2 induces angiogenesis molecular-targeting therapies xenograft mouse model 2 μg anti-lrg-1 antibody lrg-1-induced malignant behavior growth factors play epithelial-mesenchymal transition yi-fan zhang glioma cell lines akt/mmp-2 signalling lrg-1-mediated malignant behavior lrg1 promotes angiogenesis erbb signalling network lrg-1-mediated malignant behaviors specific pathogen-free lrg1 promotes proliferation mapk signaling pathway privacy choices/manage cookies p38/mapk signaling subsequent regression analysis independent prognostic factor cell signaling technology key signaling pathways

Schema {🗺️}

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         headline:LRG-1 promotes pancreatic cancer growth and metastasis via modulation of the EGFR/p38 signaling
         description:The abnormal expression of leucine-rich-alpha-2-glycoprotein 1 (LRG-1) is reported to be associated with multiple malignancies, but its role in the progression of pancreatic ductal adenocarcinoma (PDAC) remains to be determined. The expression of LRG-1 was assessed in PDAC tissues by RT-PCR, Western blot and immunohistochemistry. LRG-1-silenced or overexpressed cell lines were constructed using shRNA or LRG-1-overexpressing plasmids. EdU incorporation assay, Transwell invasion and wound-healing assays were performed to evaluate the proliferation, invasion and migration of PDAC cells. In addition, protein expression of the mitogen-activated protein kinase (MAPK) pathway was detected using Western blot. Finally, Co-immunoprecipitation assay was conducted in search of the potential interaction between LRG-1 and epidermal growth factor receptor (EGFR). The expression of LRG-1 in PDAC tissue was significantly higher than that in adjacent normal tissue, and high LRG-1 expression predicted poor survival and a late tumor stage. In addition, LRG-1 markedly promoted the viability, proliferation, migration and invasion of PDAC cells in vitro and facilitated tumor growth in vivo. More importantly, we revealed that these bioactivities of LRG-1 might result from its selective interaction with EGFR, which might further activate the p38/MAPK signaling pathways. LRG-1 may prove to be a promising biomarker for predicting prognosis of PDAC patients. Inhibition of LRG-1 or its downstream pathway could be a potential therapeutic target for the treatment of PDAC.
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      description:The abnormal expression of leucine-rich-alpha-2-glycoprotein 1 (LRG-1) is reported to be associated with multiple malignancies, but its role in the progression of pancreatic ductal adenocarcinoma (PDAC) remains to be determined. The expression of LRG-1 was assessed in PDAC tissues by RT-PCR, Western blot and immunohistochemistry. LRG-1-silenced or overexpressed cell lines were constructed using shRNA or LRG-1-overexpressing plasmids. EdU incorporation assay, Transwell invasion and wound-healing assays were performed to evaluate the proliferation, invasion and migration of PDAC cells. In addition, protein expression of the mitogen-activated protein kinase (MAPK) pathway was detected using Western blot. Finally, Co-immunoprecipitation assay was conducted in search of the potential interaction between LRG-1 and epidermal growth factor receptor (EGFR). The expression of LRG-1 in PDAC tissue was significantly higher than that in adjacent normal tissue, and high LRG-1 expression predicted poor survival and a late tumor stage. In addition, LRG-1 markedly promoted the viability, proliferation, migration and invasion of PDAC cells in vitro and facilitated tumor growth in vivo. More importantly, we revealed that these bioactivities of LRG-1 might result from its selective interaction with EGFR, which might further activate the p38/MAPK signaling pathways. LRG-1 may prove to be a promising biomarker for predicting prognosis of PDAC patients. Inhibition of LRG-1 or its downstream pathway could be a potential therapeutic target for the treatment of PDAC.
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