Obesity-Associated ECM Remodeling in Cancer Progression.

Obesity-Associated ECM Remodeling in Cancer Progression.
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肥胖相关的细胞外基质重塑在癌症进展中的作用

DOI:
10.3390/cancers14225684
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发表时间:
2022-11-19
期刊:
影响因子:
5.2
通讯作者:
Xu, Ren
Xu, Ren
中科院分区:
医学2区
文献类型:
--
作者:
Li, Junyan;Xu, Ren

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积累的证据表明,脂肪细胞可以转化或去分化为肌成纤维细胞/成纤维细胞样细胞,在肥胖相关的细胞外基质(ECM)重塑和癌症进展中发挥重要作用。本综述总结了肥胖相关癌症进展过程中脂肪细胞可塑性的最新进展,以及肥胖相关 ECM 重塑在癌症进展中的功能和调节。脂肪组织是一种能量储存和内分泌器官,正在成为 ECM 重塑的重要参与者。纤维化是肥胖脂肪组织的标志之一,其特点是细胞外基质过度沉积和胶原蛋白排列增强。肥胖脂肪组织中的脂肪细胞和肌成纤维细胞产生多种 ECM 成分和 ECM 相关酶。来自谱系追踪模型和单细胞分析的数据表明脂肪细胞可以转化或去分化为肌成纤维细胞/成纤维细胞样细胞。这种去分化过程已在正常组织发育和病理条件下观察到,例如皮肤纤维化、伤口愈合和癌症发展。积累的证据表明,脂肪细胞去分化和肌成纤维细胞/成纤维细胞在肥胖相关的 ECM 重塑和癌症进展中发挥着至关重要的作用。在这篇综述中,我们总结了肥胖相关 ECM 重塑的最新进展、脂肪细胞去分化的机制以及肥胖相关 ECM 重塑在癌症进展中的功能。
Accumulated evidence has demonstrated that adipocytes can transform or de-differentiate into myofibroblast/fibroblast-like cells, which play vital roles in obesity-related extracellular matrix (ECM) remodeling and cancer progression. This review summarizes recent progress in adipocyte plasticity during obesity-related cancer progression and the function and regulation of obesity-associated ECM remodeling in cancer progression. Adipose tissue, an energy storage and endocrine organ, is emerging as an essential player for ECM remodeling. Fibrosis is one of the hallmarks of obese adipose tissue, featuring excessive ECM deposition and enhanced collagen alignment. A variety of ECM components and ECM-related enzymes are produced by adipocytes and myofibroblasts in obese adipose tissue. Data from lineage-tracing models and a single-cell analysis indicate that adipocytes can transform or de-differentiate into myofibroblast/fibroblast-like cells. This de-differentiation process has been observed under normal tissue development and pathological conditions such as cutaneous fibrosis, wound healing, and cancer development. Accumulated evidence has demonstrated that adipocyte de-differentiation and myofibroblasts/fibroblasts play crucial roles in obesity-associated ECM remodeling and cancer progression. In this review, we summarize the recent progress in obesity-related ECM remodeling, the mechanism underlying adipocyte de-differentiation, and the function of obesity-associated ECM remodeling in cancer progression.
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