Tumor necrosis: A synergistic consequence of metabolic stress and inflammation.

Tumor necrosis: A synergistic consequence of metabolic stress and inflammation.
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DOI:
10.1002/bies.202100029
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发表时间:
2021-07
期刊:
BioEssays : news and reviews in molecular, cellular and developmental biology
影响因子:
--
通讯作者:
Li W
Li W
中科院分区:
其他
文献类型:
--
作者:
Yee PP;Li W

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肿瘤坏死是一种常见的组织学特征,是各种癌症的不良预后预测因子。尽管其具有重要的临床意义,但由于缺乏适当的临床前模型,肿瘤坏死的潜在机制在很大程度上仍不清楚。我们认为肿瘤坏死是代谢应激和炎症协同作用的结果,导致氧化应激诱导的细胞死亡,如铁凋亡。作为肿瘤扩张的自然结果,肿瘤细胞不可避免地被剥夺了血管供应,导致氧气和营养物质的剥夺。由此产生的代谢应激通常被认为是肿瘤坏死的原因。最近的研究发现,免疫细胞,如中性粒细胞,当被招募到肿瘤时,可以直接触发肿瘤细胞中的铁凋亡,这表明免疫细胞可以参与放大肿瘤坏死。本文将讨论肿瘤坏死发展的潜在机制及其对肿瘤进展的影响以及对肿瘤的免疫反应。
Tumor necrosis is a common histological feature and poor prognostic predictor in various cancers. Despite its significant clinical implications, the mechanism underlying tumor necrosis remains largely unclear due to lack of appropriate pre-clinical modeling. We propose that tumor necrosis is a synergistic consequence of metabolic stress and inflammation, which lead to oxidative stress-induced cell death, such as ferroptosis. As a natural consequence of tumor expansion, tumor cells are inevitably stripped of vascular supply, resulting in deprivation of oxygen and nutrients. The resulting metabolic stress has commonly been considered the cause of tumor necrosis. Recent studies found that immune cells, such as neutrophils, when recruited to tumors, can directly trigger ferroptosis in tumor cells, suggesting that immune cells can be involved in amplifying tumor necrosis. This article will discuss potential mechanisms underlying tumor necrosis development and its impact on tumor progression as well as the immune response to tumors.
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