肺癌（LCa）是世界上最常见的恶性肿瘤，每年导致数百万人死亡。已经确定长非编码 RNA MIR210HG 在 LCa 中过度表达；然而，有必要对其在 LCA 中的生物学作用进行更全面的研究。本研究旨在验证 LCa 组织和细胞中的 MIR210H 水平。使用定量实时聚合酶链反应（qRT-PCR）和/或蛋白质印迹评估指定基因的表达。使用 3-(4,5-二甲基噻唑-2-基)-2,5-二苯基溴化四唑 (MTT)、集落形成、伤口愈合和 Transwell 测定来测量 LCa 细胞的活力、增殖、迁移和侵袭， 分别。通过甲基化特异性PCR测定LCa细胞的甲基化水平；此外，还进行染色质免疫沉淀或RNA免疫沉淀测定，以确定DNA甲基转移酶1（DNMT1）和含有CRB2样3（SH3GL3）启动子的SH3结构域之间的靶向关系以及DNMT1和MIR210HG之间的相互作用。我们的研究结果揭示了 LCa 组织和细胞中 MIR210HG 的上调以及 SH3GL3 表达的减少。 MIR210HG 的敲低或 SH3GL3 的过表达抑制了细胞的增殖、迁移和侵袭能力。 DNMT1 与 SH3GL3 启动子区域结合，MIR210HG 通过招募 DNMT1 来抑制 SH3GL3 的转录。这些发现表明，MIR210HG 通过将 DNMT1 招募到 SH3GL3 启动子区域来抑制 SH3GL3 转录，从而促进 LCa 细胞生长和转移。© 2023 作者。约翰·威利出版的《高雄医学科学杂志》

Lung cancer (LCa), the most frequent malignancy worldwide, causes millions of mortalities each year. Overexpression of the long noncoding RNA MIR210HG in LCa has been established; however, a more comprehensive investigation into its biological role within LCa is imperative. This study aimed to validate the MIR210H levels in LCa tissues and cells. The expression of indicated genes was evaluated using quantitative real-time polymerase chain reaction (qRT-PCR) and/or Western blotting. The viability, proliferation, migration, and invasion of LCa cells were measured using the 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT), colony formation, wound healing, and transwell assays, respectively. The methylation levels of LCa cells were determined via methylation-specific PCR; additionally, chromatin immunoprecipitation or RNA immunoprecipitation assays were performed to determine the targeting relationship between DNA methyltransferase 1 (DNMT1) and the SH3-domain containing CRB2 like 3 (SH3GL3) promoters and the interaction between DNMT1 and MIR210HG, respectively. Our findings revealed the upregulation of MIR210HG, coupled with a diminished expression of SH3GL3 in LCa tissues and cells. Knockdown of MIR210HG or overexpression of SH3GL3 suppressed the proliferative, migratory, and invasive capacities of the cells. DNMT1 bound to the SH3GL3 promoter region, and MIR210HG inhibited the transcription of SH3GL3 by recruiting DNMT1. These findings indicate that MIR210HG facilitates LCa cell growth and metastasis by repressing SH3GL3 transcription via the recruitment of DNMT1 to the SH3GL3 promoter region.© 2023 The Authors. The Kaohsiung Journal of Medical Sciences published by John Wiley & Sons Australia, Ltd on behalf of Kaohsiung Medical University.