ArticleMediators of inflammation2012
The EGF receptor and HER2 participate in TNF-α-dependent MAPK activation and IL-8 secretion in intestinal epithelial cells.
Article in Mediators of inflammation, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 31 citations in OpenAlex.
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- Inhibition of cell invasion and migration by targeting matrix metalloproteinase-9 expression via sirtuin 6 silencing in human breast cancer cells.Scientific reports · 2022Article
- Molecular regulation after mucosal injury and regeneration in ulcerative colitis.Frontiers in molecular biosciences · 2022Review
- TNF-α-induced sympathetic excitation requires EGFR and ERK1/2 signaling in cardiovascular regulatory regions of the forebrain.American journal of physiology. Heart and circulatory physiology · 2021Article
- Ethyl pyruvate inhibits LPS induced IPEC-J2 inflammation and apoptosis through p38 and ERK1/2 pathways.Cell cycle (Georgetown, Tex.) · 2019Article
- Regulation of the hypoxic tumor environment in hepatocellular carcinoma using RNA interference.Cancer cell international · 2017Review
- Bile acids regulate intestinal cell proliferation by modulating EGFR and FXR signaling.American journal of physiology. Gastrointestinal and liver physiology · 2016Article
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- Pathogenic Lifestyles ofFrontiers in cellular and infection microbiology · 2016Article
- Adenovirus E4-ORF1 Dysregulates Epidermal Growth Factor and Insulin/Insulin-Like Growth Factor Receptors To Mediate Constitutive Myc Expression.Journal of virology · 2015Article
- Inflammation-induced desmoglein-2 ectodomain shedding compromises the mucosal barrier.Molecular biology of the cell · 2015Article
- Establishment and characterization of cetuximab resistant head and neck squamous cell carcinoma cell lines: focus on the contribution of the AP-1 transcription factor.American journal of cancer research · 2015Article
- Disruption of CXCR2-mediated MDSC tumor trafficking enhances anti-PD1 efficacy.Science translational medicine · 2014Article
- The inflammatory cytokine TNFα cooperates with Ras in elevating metastasis and turns WT-Ras to a tumor-promoting entity in MCF-7 cells.BMC cancer · 2014Article
- Enterococcus faecalis from healthy infants modulates inflammation through MAPK signaling pathways.PloS one · 2014Article
- The complex function of hsp70 in metastatic cancer.Cancers · 2013Article
- Comparative proteome analysis of Tumor necrosis factor α-stimulated human Vascular Smooth Muscle Cells in response to melittin.Proteome science · 2013Article
- Progression of luminal breast tumors is promoted by ménage à trois between the inflammatory cytokine TNFα and the hormonal and growth-supporting arms of the tumor microenvironment.Mediators of inflammation · 2013Article
- Anti-epidermal growth factor receptor therapy in head and neck squamous cell carcinoma: focus on potential molecular mechanisms of drug resistance.The oncologist · 2013Review
- Paeoniflorin protects against ischemia-induced brain damages in rats via inhibiting MAPKs/NF-κB-mediated inflammatory responses.PloS one · 2012Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
TNF-α activates multiple mitogen-activated protein kinase (MAPK) cascades in intestinal epithelial cells (IECs) leading to the secretion of interleukin 8 (IL-8), a neutrophil chemoattractant and an angiogenic factor with tumor promoting properties. As the epidermal growth factor receptor (EGFR) is a known transducer of proliferative signals and a potent activator of MAPKs, we hypothesized that the EGFR participates in TNF-dependent MAPK activation and IL-8 secretion by intestinal epithelial cells (IECs). We show that the EGFR is tyrosine-phosphorylated following treatment of IECs (HT-29 and IEC-6) with TNF-α. This requires EGFR autophosphorylation as it was blocked by the EGFR kinase inhibitor AG1478. Autophosphorylation was also inhibited by both a Src-kinase inhibitor and the metalloproteinase inhibitor batimastat. TNF treatment of IECs resulted in the accumulation of soluble TGF-α; treatment of IECs with batimastat suppressed TGF-α release and immunoneutralization of TGF-α resulted in decreased EGFR and ERK phosphorylations. TNF-α treatment of IECs resulted in an association between EGFR and HER2 and inhibition of HER2 using a specific inhibitor AG879 in combination with AG1478-suppressed TNF-α-dependent ERK phosphorylation and IL-8 release. Downregulation of HER2 via siRNA resulted in a significant decrease in ERK phosphorylation and a 50% reduction in IL-8 secretion.
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