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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: BACKGROUND, METHODS, RESULTS. Meshes: Apoptosis, Biomarkers, Blotting, Western, Caveolin 1, Cell Proliferation, Cells, Cultured, Fluorescent Antibody Technique, Gene Expression Profiling, Humans, Interleukin-6, JNK Mitogen-Activated Protein Kinases, Lipopolysaccharides, Mammary Glands, Human, Oligonucleotide Array Sequence Analysis, Phosphorylation, Signal Transduction, Toll-Like Receptor 4, p38 Mitogen-Activated Protein Kinases.
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Is caveolin-1 , through its ability to negatively regulate TLR4 , a crucial determinant of MAPK activation in LPS-challenged mammary epithelial cells? Context: To explore the role of caveolin-1(CAV-1) gene silencing on MAPK activation in lipopolysaccharide (LPS)-challenged human mammary epithelial cells. We established a MCF-10ACE of CAV-1 gene silencing from human mammary epithelial cell line MCF-10A by RNAi technology. DNA Microarray were used to detect the expression of inflammation-associated genes in MCF-10ACE. Western blotting was used to examine the activation of MAPK in lipopolysaccharide(LPS)-challenged MCF-10A and MCF-10ACE. Moreover, immunofluorescence and Western bloting were performed to detect the co-localization of CAV-1 and toll-like receptor 4 (TLR4) in human mammary epithelial cells. MCF-10ACE exhibited significant increases in inflammation-associated gene expression, especially IL-6 (~7-fold) and IL6R (~17-fold). In addition, LPS-induced p38 MAPK and JNK MAPK activation was significantly increased in MCF-10ACE. Furthermore, CAV-1 co- localized with TLR4 and appeared a negative correlation trend.
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CAV-1 gene silencing promotes MAPK activation via TLR4 signaling in human mammary epithelial cells response to LPS. Final Decision: yes