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DNMT3B 介导的 FAM111B 甲基化促进甲状腺乳头状瘤糖酵解、生长和转移。

DNMT3B-mediated FAM111B methylation promotes papillary thyroid tumor glycolysis, growth and metastasis.

机构信息

Department of Endocrinology, the First Medical Center of PLA General Hospital, Beijing, China.

Department of Genetic Engineering, Beijing Institute of Biotechnology, Beijing, China.

出版信息

Int J Biol Sci. 2022 Jul 4;18(11):4372-4387. doi: 10.7150/ijbs.72397. eCollection 2022.

DOI:10.7150/ijbs.72397
PMID:35864964
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9295055/
Abstract

Over the past decades, the incidence of thyroid cancer (TC) rapidly increased all over the world, with the papillary thyroid cancer (PTC) accounting for the vast majority of TC cases. It is crucial to investigate novel diagnostic and therapeutic targets for PTC and explore more detailed molecular mechanisms in the carcinogenesis and progression of PTC. Based on the TCGA and GEO databases, FAM111B is downregulated in PTC tissues and predicts better prognosis in PTC patients. FAM111B suppresses the growth, migration, invasion and glycolysis of PTC both and . Furthermore, estrogen inhibits FAM111B expression by DNMT3B methylation via enhancing the recruitment of DNMT3B to FAM111B promoter. DNMT3B-mediated FAM111B methylation accelerates the growth, migration, invasion and glycolysis of PTC cells. In clinical TC patient specimens, the expression of FAM111B is inversely correlated with the expressions of DNMT3B and the glycolytic gene PGK1. Besides, the expression of FAM111B is inversely correlated while DNMT3B is positively correlated with glucose uptake in PTC patients. Our work established E2/DNMT3B/FAM111B as a crucial axis in regulating the growth and progression of PTC. Suppression of DNMT3B or promotion of FAM111B will be potential promising strategies in the estrogen induced PTC.

摘要

在过去的几十年中，全球范围内甲状腺癌 (TC) 的发病率迅速上升，其中甲状腺乳头状癌 (PTC) 占 TC 病例的绝大多数。研究 PTC 的新的诊断和治疗靶点，探讨 PTC 发生和发展过程中更详细的分子机制至关重要。基于 TCGA 和 GEO 数据库，FAM111B 在 PTC 组织中下调，并预测 PTC 患者的预后更好。FAM111B 通过抑制生长、迁移、侵袭和糖酵解来抑制 PTC 的生长、迁移、侵袭和糖酵解。此外，雌激素通过 DNMT3B 甲基化抑制 FAM111B 表达，从而增强 DNMT3B 向 FAM111B 启动子的募集。DNMT3B 介导的 FAM111B 甲基化加速了 PTC 细胞的生长、迁移、侵袭和糖酵解。在临床 TC 患者标本中，FAM111B 的表达与 DNMT3B 和糖酵解基因 PGK1 的表达呈负相关。此外，在 PTC 患者中，FAM111B 的表达与葡萄糖摄取呈负相关，而 DNMT3B 的表达与葡萄糖摄取呈正相关。我们的工作建立了 E2/DNMT3B/FAM111B 作为调节 PTC 生长和进展的关键轴。抑制 DNMT3B 或促进 FAM111B 将成为雌激素诱导的 PTC 的潜在有前途的策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/012a/9295055/c0d2236a2e9b/ijbsv18p4372g007.jpg
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