%0 Journal Article %T Caveolin-1, Through its Ability to Negatively Regulate TLR4, is a Crucial Determinant of MAPK Activation in LPS-challenged Mammary Epithelial Cells %J Asian Pacific Journal of Cancer Prevention %I West Asia Organization for Cancer Prevention (WAOCP), APOCP's West Asia Chapter. %Z 1513-7368 %D 2013 %\ 04/01/2013 %V 14 %N 4 %P 2295-2299 %! Caveolin-1, Through its Ability to Negatively Regulate TLR4, is a Crucial Determinant of MAPK Activation in LPS-challenged Mammary Epithelial Cells %K Cav-1 %K LPS-MAPK pathway %K TLR4 %K mastitis %K breast cancer %R %X Background: To explore the role of caveolin-1(CAV-1) gene silencing on MAPK activation in lipopolysaccharide(LPS)-challenged human mammary epithelial cells. Methods: We established a MCF-10ACE of CAV-1 genesilencing from human mammary epithelial cell line MCF-10A by RNAi technology. DNA Microarray wereused to detect the expression of inflammation-associated genes in MCF10ACE. Western blotting was used toexamine 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-likereceptor 4 (TLR4) in human mammary epithelial cells. Results: MCF-10ACE exhibited significant increases ininflammation-associated gene expression, especially IL-6 (~7-fold) and IL6R (~17-fold). In addition, LPS-inducedp38 MAPK and JNK MAPK activation was significantly increased in MCF-10ACE. Furthermore, CAV-1 colocalizedwith TLR4 and appeared a negative correlation trend. Conclusion: CAV-1 gene silencing promotesMAPK activation via TLR4 signaling in human mammary epithelial cells response to LPS. %U https://journal.waocp.org/article_27406_8f359eca7463bbefd75e3149eca81083.pdf