Snail1控制转移过程中的协同细胞可塑性

J. Baulida
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引用次数: 2

摘要

癌症的死亡率与肿瘤细胞扩散并严重影响其他组织和器官的能力密切相关。肿瘤细胞积累的基因突变和肿瘤与宿主细胞之间的交叉信号传导是转移形成的基础。癌症激活的成纤维细胞(CAFs)是一种被肿瘤信号激活的宿主成纤维细胞,它可以通过旁分泌信号(分泌扩散分子)和机械信号(改变基质的组成和组织)改变肿瘤细胞的行为。这些成纤维细胞类似于伤口愈合过程中产生的肉芽组织中的肌成纤维细胞(MFs),后者产生一种富含信号分子和交联细胞外纤维的刚性结缔组织基质。结缔组织增生有利于恶性肿瘤细胞的特性,如移动性、干性,甚至抵抗药物损伤[1]。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Snail1 controls cooperative cell plasticity during metastasis
Mortality in cancer is strongly associated with the capacity of tumor cells to spread and critically affect other tissues and organs. Genetic mutations accumulated by tumor cells and cross-signaling between tumor and host cells underlie the formation of metastasis. Cancer-activated fibroblasts (CAFs), which are host fibroblasts activated by tumor signaling, can alter tumor cell behavior by both paracrine signaling (secreting diffusible molecules) and mechanical signaling (modifying the composition and organization of the stroma). These fibroblasts resemble myofibroblasts (MFs) of the granulation tissue generated during wound healing, which produce a rigid desmoplastic stroma rich in signaling molecules and cross-linked extracellular fibers. Desmoplasia favors malignant tumor cell properties such as mobility, stemness, and even resistance to pharmacological insults [1].
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