TET1 通过调节自噬抑制宫颈癌细胞的迁移和侵袭。

IF 2.9 3区 生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY
Epigenetics Pub Date : 2024-12-01 Epub Date: 2024-03-03 DOI:10.1080/15592294.2024.2323751
Ji Ren, Xiuying Chen, Jing Li, Yuxin Zan, Shan Wang, Yujie Tan, Yan Ding
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引用次数: 0

摘要

甲基化修饰在调节基因表达和各种生物过程中发挥着重要作用。去甲基化酶 TET1 的沉默会影响关键癌基因或肿瘤抑制基因的表达,从而导致肿瘤的形成。然而,TET1如何影响宫颈癌的进展尚待阐明。在这项研究中,我们发现 TET1 在宫颈癌组织中的表达明显下调。在功能上,TET1 在宫颈癌细胞中的敲除可促进细胞增殖、迁移、侵袭、宫颈异种移植瘤的形成和 EMT。相反,TET1 的过表达可以逆转上述过程。此外,TET1 基因敲除后,宫颈癌细胞的自噬水平也会提高。从机理上讲,甲基化DNA免疫沉淀(MeDIP)测序和MeDIP定量实时PCR发现,TET1介导了自噬启动子区域的甲基化。这些研究结果表明,TET1通过改变NKRF或HIST1H2AK的甲基化水平来影响宫颈癌细胞的自噬,但具体机制还有待进一步研究。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
TET1 inhibits the migration and invasion of cervical cancer cells by regulating autophagy.

Methylation modifications play pertinent roles in regulating gene expression and various biological processes. The silencing of the demethylase enzyme TET1 can affect the expressions of key oncogenes or tumour suppressor genes, thus contributing to tumour formation. Nonetheless, how TET1 affects the progression of cervical cancer is yet to be elucidated. In this study, we found that the expression of TET1 was significantly downregulated in cervical cancer tissues. Functionally, TET1 knockdown in cervical cancer cells can promote cell proliferation, migration, invasion, cervical xenograft tumour formation and EMT. On the contrary, its overexpression can reverse the aforementioned processes. Moreover, the autophagy level of cervical cancer cells can be enhanced after TET1 knockdown. Mechanistically, methylated DNA immunoprecipitation (MeDIP)-sequencing and MeDIP quantitative real-time PCR revealed that TET1 mediates the methylation of autophagy promoter regions. These findings suggest that TET1 affects the autophagy of cervical cancer cells by altering the methylation levels of NKRF or HIST1H2AK, but the specific mechanism needs to be investigated further.

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来源期刊
Epigenetics
Epigenetics 生物-生化与分子生物学
CiteScore
6.80
自引率
2.70%
发文量
82
审稿时长
3-8 weeks
期刊介绍: Epigenetics publishes peer-reviewed original research and review articles that provide an unprecedented forum where epigenetic mechanisms and their role in diverse biological processes can be revealed, shared, and discussed. Epigenetics research studies heritable changes in gene expression caused by mechanisms others than the modification of the DNA sequence. Epigenetics therefore plays critical roles in a variety of biological systems, diseases, and disciplines. Topics of interest include (but are not limited to): DNA methylation Nucleosome positioning and modification Gene silencing Imprinting Nuclear reprogramming Chromatin remodeling Non-coding RNA Non-histone chromosomal elements Dosage compensation Nuclear organization Epigenetic therapy and diagnostics Nutrition and environmental epigenetics Cancer epigenetics Neuroepigenetics
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