We are analyzing https://link.springer.com/article/10.1007/s13277-014-2717-z.

Title:
The CCL2/CCR2 axis enhances IL-6-induced epithelial-mesenchymal transition by cooperatively activating STAT3-Twist signaling | Tumor Biology
Description:
The pattern of secreted factors in the tumor microenvironment has been shown to initiate tumor epithelial-mesenchymal transition (EMT); however, little is known about their interplay undergoing this phenotypic switch. In this study, we revealed obvious coactions of cytokine IL-6 and chemokine CCL2 during EMT induction. We found that IL-6 effectively induced EMT and promoted tumor cell invasion, which could be markedly enhanced by addition of CCL2 in a CCR2-dependent manner. IL-6 and CCL2 induced each other and cooperatively elicited STAT3 phosphorylation; conversely, STAT3 regulated the production of IL-6 and CCL2, thus constituting a positive feedback loop to maintain and amplify STAT3 signaling, consequently promoting additional EMT events. Furthermore, CCL2 greatly enhanced IL-6-induced EMT events mainly by upregulating the expression of Twist. Genetic or pharmacological inhibition of STAT3 disrupted STAT3-centered loop and markedly suppressed Twist expression as well as IL-6/CCL2-mediated EMT induction. Thus, our findings highlighted the synergy of the two secreted factors of tumor microenvironment, in regulating transformed properties of non-small cell lung cancer (NSCLC).
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Keywords {🔍}

pubmed, article, google, scholar, cas, cancer, cell, epithelialmesenchymal, tumor, transition, metastasis, central, emt, signaling, ccl, stat, lung, cells, wei, chen, microenvironment, res, transitions, privacy, cookies, content, expression, twist, access, department, hospital, china, information, publish, research, search, ilinduced, gao, han, nonsmall, mesenchymal, stem, clin, biol, mol, data, log, journal, biology, cooperatively,

Topics {✒️}

il-6-induced epithelial-mesenchymal transition ccl2/ccr2-induced stat3 activation month download article/chapter epithelial-mesenchymal transition phenotype inducing epithelial-mesenchymal transition jak-stat3-snail signaling pathway inflammation-induced cell migration il-6/ccl2-mediated emt induction epithelial-mesenchymal transition nf-kappab e-cadherin promotes metastasis il-6/sil-6r complex cancer stem cells epithelial-mesenchymal transitions stem cell states full article pdf stem cell traits circulating tumor cells il-6 promotes head amplify stat3 signaling neck tumor metastasis cancer cell metastasis ccr2-dependent manner epithelial-mesenchymal promote cancer metastasis ccr2 expression correlates privacy choices/manage cookies related subjects clin exp metastasis tumor microenvironment heldin ch twist1 induces ccl2 lung adenocarcinoma growth tgf-beta signaling il6-mediated suppression enhanced macrophage recruitment monocyte chemoattractant protein-1 ccl2 induced nat rev cancer cancer immunol immunother prostate cancer progression prostate intraepithelial neoplasia mesenchymal states embo mol med clin cancer res mol cancer res article chen positive feedback loop mesenchymal transitions exp cell res

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         description:The pattern of secreted factors in the tumor microenvironment has been shown to initiate tumor epithelial-mesenchymal transition (EMT); however, little is known about their interplay undergoing this phenotypic switch. In this study, we revealed obvious coactions of cytokine IL-6 and chemokine CCL2 during EMT induction. We found that IL-6 effectively induced EMT and promoted tumor cell invasion, which could be markedly enhanced by addition of CCL2 in a CCR2-dependent manner. IL-6 and CCL2 induced each other and cooperatively elicited STAT3 phosphorylation; conversely, STAT3 regulated the production of IL-6 and CCL2, thus constituting a positive feedback loop to maintain and amplify STAT3 signaling, consequently promoting additional EMT events. Furthermore, CCL2 greatly enhanced IL-6-induced EMT events mainly by upregulating the expression of Twist. Genetic or pharmacological inhibition of STAT3 disrupted STAT3-centered loop and markedly suppressed Twist expression as well as IL-6/CCL2-mediated EMT induction. Thus, our findings highlighted the synergy of the two secreted factors of tumor microenvironment, in regulating transformed properties of non-small cell lung cancer (NSCLC).
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      description:The pattern of secreted factors in the tumor microenvironment has been shown to initiate tumor epithelial-mesenchymal transition (EMT); however, little is known about their interplay undergoing this phenotypic switch. In this study, we revealed obvious coactions of cytokine IL-6 and chemokine CCL2 during EMT induction. We found that IL-6 effectively induced EMT and promoted tumor cell invasion, which could be markedly enhanced by addition of CCL2 in a CCR2-dependent manner. IL-6 and CCL2 induced each other and cooperatively elicited STAT3 phosphorylation; conversely, STAT3 regulated the production of IL-6 and CCL2, thus constituting a positive feedback loop to maintain and amplify STAT3 signaling, consequently promoting additional EMT events. Furthermore, CCL2 greatly enhanced IL-6-induced EMT events mainly by upregulating the expression of Twist. Genetic or pharmacological inhibition of STAT3 disrupted STAT3-centered loop and markedly suppressed Twist expression as well as IL-6/CCL2-mediated EMT induction. Thus, our findings highlighted the synergy of the two secreted factors of tumor microenvironment, in regulating transformed properties of non-small cell lung cancer (NSCLC).
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