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首页> 外文期刊>Cell cycle >Inflammation and autophagy conspire to promote tumor growth.
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Inflammation and autophagy conspire to promote tumor growth.

机译：炎症和自噬共同促进肿瘤生长。

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Considerable pre-dinical and clinical evidence links the production of inflammatory cyto-kines in the tumor microenvironment to cancer progression. Although the mechanisms that mediate the interaction of tumor cells and their microenvironment are currently under investigation, it is clear that paracrine signals from evolving tumors induce epigenetic changes in surrounding stromal fibroblasts.' A model has recently been proposed in which cancer cells induce oxidative stress and subsequent autophagy in adjacent fibroblasts, which, in turn, generate recycled nutrients that support tumor growth.Recent studies reveal that that bi-directional cytokine signaling networks between tumor and stromal cells mediate tumor progression, metastasis and therapeutic resistance. In particular, inflammatory cytokines, including IL6 and IL8, have been strongly associated with these processes. Martinez-Outschoom et al. extend this previous work by linking the generation of inflammatory cytokines with autophagy. They demonstrate that oxidative stress generated by tumor cells upon co-culture with fibroblasts induces autophagy as a consequence of downregu-lation of caveolin-1 expression and upreg-ulation of inflammatory cytokines (Fig. 1).
机译：大量的常规和临床证据将肿瘤微环境中炎性细胞因子的产生与癌症进展联系起来。尽管目前正在研究介导肿瘤细胞及其微环境相互作用的机制，但很明显，来自不断演变的肿瘤的旁分泌信号诱导周围基质成纤维细胞的表观遗传学改变。最近有人提出了一种模型，其中癌细胞在邻近的成纤维细胞中诱导氧化应激并随后自噬，进而产生支持肿瘤生长的再循环养分。最近的研究表明，肿瘤与基质细胞之间的双向细胞因子信号网络介导肿瘤进展，转移和治疗抵抗力。特别地，包括IL6和IL8在内的炎性细胞因子与这些过程密切相关。 Martinez-Outschoom等。通过将炎症细胞因子的产生与自噬联系起来，扩展了以前的工作。他们证明肿瘤细胞与成纤维细胞共培养时产生的氧化应激可诱导自噬，这是小窝蛋白1表达下调和炎性细胞因子上调的结果（图1）。

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