缺氧(环境)
肿瘤微环境
肿瘤进展
癌症研究
肿瘤缺氧
转移
生物
信号转导
下调和上调
癌细胞
癌症
免疫学
医学
细胞生物学
内科学
化学
放射治疗
肿瘤细胞
有机化学
氧气
基因
生物化学
作者
Stephen Connor Purdy,Heide L. Ford
出处
期刊:Cancer Research
[American Association for Cancer Research]
日期:2024-10-01
卷期号:84 (19): 3125-3127
标识
DOI:10.1158/0008-5472.can-24-2407
摘要
Hypoxia occurs in 90% of solid tumors and is strongly associated with an increased propensity for metastasis. Hypoxia induces tumor progression largely through inducing HIF-mediated transcription, resulting in alterations to tumor cell metabolism, as well as increases in migration and invasion. Hypoxia also results in a myriad of changes to the tumor microenvironment (TME). While many studies have examined the immediate effects of hypoxia on tumor cells and the associated TME, far fewer have focused on the long-term consequences of transient reductions in oxygen. In this issue of Cancer Research, Iriondo and colleagues examined whether short-term exposure to hypoxia leads to a “hypoxic memory” in the context of breast cancer. The authors used established cell lines and circulating tumor cell lines to demonstrate that these cells harbor a hypoxic memory that sustains downregulation of IFN signaling and antigen presentation (AP) pathways that contribute to tumor progression via alterations to tumor cells and the TME. The authors further showed that cells that have experienced hypoxia maintain the reduction in IFN signaling in vivo and are more aggressive. They determined that the hypoxic memory and reduction of IFN signaling can be reversed with a histone deacetylase inhibitor, entinostat, providing a potential means to reverse hypoxia-induced suppression of IFN signaling. As suppression of IFN signaling has the potential to influence both tumor cells and the TME, the identification of a strategy to inhibit long-term suppression of IFN signaling downstream of hypoxia could prove to be an effective means to target tumor progression. See related article by Iriondo et al., p. 3141
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