RNF43 p.G659fs 通过 PI3K/AKT/mTOR 信号通路和 HLA-E 上调导致 MSI-high 结直肠癌中 NK 细胞功能障碍
RNF43 p.G659fs leads to natural killer cell dysfunction in MSI-high colorectal cancer through PI3K/AKT/mTOR signaling and HLA-E up-regulation.
CELL INTELLIGENCE · 肿瘤细胞治疗研究
肿瘤细胞治疗研究
英文原题:The epigenetic hallmarks of immune cells in cancer.
The epigenetic hallmarks of immune cells in cancer.
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靶向癌症中表观遗传机制的失调已成为一种有前景的治疗策略。尽管表观遗传疗法在阻断癌细胞方面取得了重要的理论进展,但表观遗传调控如何塑造肿瘤微环境(TME)并建立抗肿瘤免疫仍知之甚少。近年来的研究重点集中在表观遗传介导的免疫细胞命运变化,包括TME中T细胞、自然杀伤(NK)细胞、肿瘤相关巨噬细胞(TAMs)、树突状细胞(DCs)、髓源性抑制细胞(MDSCs)和B细胞的分化、扩增、募集、功能化及耗竭。在此,我们综述了关于DNA修饰、组蛋白修饰和表观转录组相关调控如何塑造多种癌症免疫细胞的最新分子和临床见解。我们还讨论了利用表观遗传疗法改善癌症免疫治疗的机会。本综述提供了癌症免疫的表观遗传学基础,并提出了联合治疗的未来方向。
Targeting the dysregulation of epigenetic mechanisms in cancer has emerged as a promising therapeutic strategy. Although the significant rationale progress of epigenetic therapies in blocking cancer cells, how epigenetic regulation shapes tumor microenvironment (TME) and establishes antitumor immunity remains less understood.
Recent study focus has been put on the epigenetic-mediated changes in the fate of immune cells, including the differentiation, expansion, recruitment, functionalization, and exhaustion of T cells, natural killer (NK) cells, tumor-associated macrophages (TAMs), dendritic cells (DCs), myeloid-derived suppressor cells (MDSCs), and B cells within the TME.
Here, we review the latest molecular and clinical insights into how DNA modifications, histone modification, and epitranscriptome-related regulations shape immune cells of various cancers.
We also discuss opportunities for leveraging epigenetic therapies to improve cancer immunotherapies. This review provides the epigenetic foundations of cancer immunity and proposes the future direction of combination therapies.
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