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首页> 外文期刊>Journal of cellular physiology. >c-Fos separation from Lamin A/C by GDF15 promotes colon cancer invasion and metastasis in inflammatory microenvironment
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c-Fos separation from Lamin A/C by GDF15 promotes colon cancer invasion and metastasis in inflammatory microenvironment

机译：c-Fos分离核纤层蛋白A / C GDF15促进结肠癌入侵和转移炎症微环境

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Inflammatory microenvironment is an important factor for promoting cancer invasion and metastasis, but the underlying molecular mechanisms remain unclear. Here, we mimicked an inflammatory microenvironment both in vitro and in vivo and investigated its effects on the invasion and metastasis of colon cancer. Moreover, colon cancer patient samples were also analyzed statistically. Conditioned medium from the differentiated macrophages induced invasion and migration of colon cancer cells in vitro, which could be reversed by the treatment of a neutralizing anti-growth differentiation factor 15 (GDF15) antibody, indicating GDF15 involvement in inflammation-induced invasiveness. Also, we observed similar effects of human recombinant GDF15 on colon cancer cells. Mechanistically, GDF15 activated c-Fos by separating it from Lamin A/C, increasing transcriptional activity of c-Fos and regulating EMT gene expressions. However, c-Fos knockdown using lentivirus shRNA plasmid inhibited GDF15-triggered invasion and migration in vitro. In vivo, inflammation caused by lipopolysaccharides obviously increased GDF15 secretion, and c-Fos knockdown reduced the lung metastasis of colon cancer cells in mice model. In addition, c-Fos expressions in patient samples were found to be associated with colon cancer metastasis and TNM stages. Taken together, GDF15 in inflammatory microenvironment induces colon cancer invasion and metastasis by regulating EMT genes by activating c-Fos, which might be a potential therapeutic target for metastatic colon cancer.
机译：炎症微环境是重要的促进癌症入侵和因素转移,但潜在的分子机制尚不清楚。炎症微环境和体外体内及其影响调查入侵和转移的结肠癌。此外,结肠癌患者样本也统计分析。分化的巨噬细胞诱导的入侵和迁移的结肠癌细胞在体外,可逆转的治疗中和抑制分化因子15 (GDF15)抗体,表明GDF15参与在inflammation-induced侵袭性。人类重组的观察到类似的效果GDF15在结肠癌细胞。GDF15激活c-Fos核纤层蛋白的方法分离A / C, c-Fos转录活动的增加和调节EMT基因表达式。使用慢病毒成分质粒c-Fos击倒抑制GDF15-triggered入侵和迁移体外。脂多糖明显增加GDF15分泌,c-Fos击倒减少了肺转移的结肠癌细胞在小鼠模型。此外,c-Fos患者样本中的表达被发现与结肠癌有关吗转移、TNM阶段。在炎症微环境诱导结肠调节EMT癌症入侵和转移基因通过激活c-Fos,这可能是一个潜在的转移性结肠癌的治疗目标癌症。

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