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氨酸甲基转移酶2D调节了头癌的免疫反应和转移

Jianchun Wu¹, Crystal Chun¹, Angelica M Lagunas¹

¹University of Illinois Cancer Center, Chicago, IL, U.S.A.

Anticancer research

|July 26, 2024

概括

基因组甲基转移酶KMT2D通过调节CCL2.2促进头部和部状细胞癌 (HNSC) 转移. 向KMT2D可能会减少HNSC中的转移和T淋巴细胞耗尽.

科学领域:

表观遗传学在表观遗传学中,表观遗传学是指表观遗传学.
癌症生物学癌症生物学
免疫学免疫学免疫学

背景情况:

在头部和部状细胞癌 (HNSC) 中,KMT2D经常发生变化.
KMT2D通过基因组甲基化调节基因表达.
瘤相关巨细胞 (TAMs) 促进HNSC生长和转移,部分原因是诱导T淋巴细胞耗尽.
CCL2是一种关键的化学激素,可以吸引TAM到瘤中.

研究的目的:

调查KMT2D在HNSC进展中的作用.
阐明KMT2D影响转移和瘤免疫微环境的机制.

主要方法:

在人类HNSC.中,KMT2D表达与淋巴结转移的相关性.
基因工程KMT2D和CCL2淘汰HNSC模型的生成和分析.
使用分子和组织学技术评估HNSC特征.
研究KMT2D对HNSC细胞增殖和迁移的影响.
基因组分析 (ChIP-seq, ATAC-seq, Hi-C) 以确定KMT2D的监管目标.

主要成果:

在HNSC中高KMT2D表达与淋巴结转移的增加相关.
在体内KMT2D缺乏会减少转移,延迟瘤发病,减缓生长.
KMT2D缺乏导致CCL2表达减少和TAM基因签名减少.
KMT2D直接针对的是CCL2基因.
在CCL2-null HNSC模型中,T淋巴细胞枯竭率降低.

结论:

KMT2D通过CCL2介导的TAM招募促进HNSC转移.
KMT2D会影响瘤微环境中的免疫反应.
KMT2D是减少HNSC转移和免疫抑制的潜在治疗标.

关键词:

在C-C基因基因基因合体2的基因基因合体.3 T细胞免疫球蛋白粘素受体3 这是T淋巴细胞.基因组学就是基因组学.淋巴细胞激活基因3 3

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