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整合甲基化组和转录组分析揭示了喉癌中 的表观遗传调控。

Integrative methylome and transcriptome analysis reveals epigenetic regulation of in laryngeal cancer.

机构信息

Department of Otorhinolaryngology Head and Neck Surgery, Eye and ENT Hospital, Fudan University, Shanghai, PR China.

Shanghai Key Clinical Disciplines of Otorhinolaryngology, Shanghai, PR China.

出版信息

Microb Genom. 2024 Mar;10(3). doi: 10.1099/mgen.0.001221.

DOI:10.1099/mgen.0.001221
PMID:38536233
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10995630/
Abstract

The aetiological mechanisms of in laryngeal cancer remain unclear. This study aimed to reveal the epigenetic signature induced by in laryngeal squamous cell carcinoma (LSCC). Combined analysis of methylome and transcriptome data was performed to address the functional role of in laryngeal cancer. Twenty-nine differentially expressed methylation-driven genes were identified by mapping the methylation levels of significant differential methylation sites to the expression levels of related genes. The combined analysis revealed that promoted Janus kinase 3 (JAK3) gene expression in LSCC. Further validation found decreased methylation and elevated expression of JAK3 in the treated LSCC cell group; abundance and JAK3 gene expression had a positive correlation in tumour tissues. This analysis provides a novel understanding of the impact of in the methylome and transcriptome of laryngeal cancer. Identification of these epigenetic regulatory mechanisms opens up new avenues for mechanistic studies to explore novel therapeutic strategies.

摘要

喉癌的病因机制仍不清楚。本研究旨在揭示 诱导喉鳞状细胞癌(LSCC)中的表观遗传特征。通过将显著差异甲基化位点的甲基化水平映射到相关基因的表达水平,对甲基组和转录组数据进行联合分析,以研究 在喉癌中的功能作用。通过映射显著差异甲基化位点的甲基化水平到相关基因的表达水平,鉴定出 29 个差异表达的甲基化驱动基因。联合分析表明, 在 LSCC 中促进了 Janus 激酶 3(JAK3)基因的表达。进一步验证发现,在处理的 LSCC 细胞组中 JAK3 的甲基化减少,表达增加;肿瘤组织中 的丰度和 JAK3 基因表达呈正相关。这项分析为 对喉癌甲基组和转录组的影响提供了新的认识。鉴定这些表观遗传调控机制为探索新的治疗策略的机制研究开辟了新的途径。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1111/10995630/7e2b6a279bf2/mgen-10-01221-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1111/10995630/3af4b6fb2258/mgen-10-01221-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1111/10995630/5a822a6c69a1/mgen-10-01221-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1111/10995630/cdc0f1a5c2a4/mgen-10-01221-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1111/10995630/5c32395b830a/mgen-10-01221-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1111/10995630/7e2b6a279bf2/mgen-10-01221-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1111/10995630/3af4b6fb2258/mgen-10-01221-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1111/10995630/5a822a6c69a1/mgen-10-01221-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1111/10995630/cdc0f1a5c2a4/mgen-10-01221-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1111/10995630/5c32395b830a/mgen-10-01221-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1111/10995630/7e2b6a279bf2/mgen-10-01221-g005.jpg

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Cancer. 2022 Sep 1;128(17):3170-3184. doi: 10.1002/cncr.34338. Epub 2022 Jul 5.
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Fusobacterium nucleatum reduces METTL3-mediated mA modification and contributes to colorectal cancer metastasis.
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Nat Commun. 2022 Mar 10;13(1):1248. doi: 10.1038/s41467-022-28913-5.
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promotes colorectal cancer cells adhesion to endothelial cells and facilitates extravasation and metastasis by inducing ALPK1/NF-κB/ICAM1 axis.通过诱导 ALPK1/NF-κB/ICAM1 轴促进结直肠癌细胞与内皮细胞黏附,并促进血管外渗和转移。
Gut Microbes. 2022 Jan-Dec;14(1):2038852. doi: 10.1080/19490976.2022.2038852.
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