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- W766868975 abstract "Breast tumor interleukin-6 (IL-6) levels increase with tumor grade, and elevated serum IL-6 correlates with poor breast cancer patient survival. Epithelial–mesenchymal transition (EMT) phenotypes such as impaired E-cadherin expression or aberrant vimentin induction are associated with enhanced metastasis and unfavorable clinical outcome in breast cancer. Despite this fact, few tumor microenvironment-derived extracellular signaling factors capable of provoking such a phenotypic transition have been identified. In this study, we showed that IL-6 exhibited an EMT phenotype characterized. Moreover, we report that the induction of an EMT by IL-6 results in the acquisition of mesenchymal traits and in the expression of cancer stem cells (CSCs) markers. Many beneficial properties have been attributed to 2-phenylnaphthyridin-4-one derivatives, including inhibition of tubulin polymerization etc. Here, we found that 2-phenylnaphthyridin-4-one derivatives could repress IL-6 induced EMT phenotype and cancer stem cell markers through repressing Jak2/STAT3 signaling pathway. LYF-11 also effectively inhibited IL6-induced decrease of E-cadherin and increase of vimentin via down-regulation of phosphorylated Jak2 and STAT3. Briefly, our results suggest that a connection between IL-6 receptor activity and phospho-STAT3 protein expression, and suggest that LYF-11 is a potential compound for breast cancer therapy by targeting major components of Jak2/STAT3 signaling pathway." @default.
- W766868975 created "2016-06-24" @default.
- W766868975 creator A5049335821 @default.
- W766868975 date "2011-01-01" @default.
- W766868975 modified "2023-09-24" @default.
- W766868975 title "2-phenylnaphthyridin-4-one 衍生物抑制Interleukin-6誘發人類乳癌上皮細胞轉換為間質細胞之研究" @default.
- W766868975 hasPublicationYear "2011" @default.
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