Objective. Increased expression of KDM1A and decreased expression of DACT1 in cervical cancer cells were noticed in a previous study. This study is aimed at exploring the mechanism behind the KDM1A regulation on DACT1 in cervical cancer cells. Methods. The expression profile of KDM1A and DACT1 in cervical cancer tissues was searched in TCGA database. In vitro experiments verified the effect of KDM1A and DACT1 on proliferation and migration ability of cervical cancer cell lines after cell transfection. The interaction of KDM1A with HDAC1 was identified by coimmunoprecipitation (Co-IP). The expression levels of KDM1A and DACT1 in cervical cancer cell lines were determined by qRT-PCR and western blot. Results. TCGA database showed that cervical cancer tissues had elevated expression of KDM1A and decreased expression of DACT1, which was consistent with the observation in cervical cancer cell lines. KDM1A was found to negatively regulate DACT1 through histone deacetylation. Meanwhile, the downregulation of KDM1A or overexpression of DACT1 could suppress the cell proliferation and migration ability in HeLa and SiHa cells. Cotransfection of KDM1A and DACT1 overexpression could reverse the increased cell proliferation and migration ability induced by KDM1A overexpression. Conclusion. KDM1A can downregulate DACT1 expression through histone deacetylation and therefore suppress the proliferation and migration of cervical cancer cells.

中文翻译：

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KDM1A调控组蛋白去乙酰化抑制宫颈癌增殖和迁移中的DACT1

客观。在先前的研究中注意到宫颈癌细胞中 KDM1A 的表达增加和 DACT1 的表达减少。本研究旨在探索 KDM1A 调控宫颈癌细胞中 DACT1 的机制。方法。在TCGA数据库中检索KDM1A和DACT1在宫颈癌组织中的表达谱。体外实验验证了KDM1A和DACT1对细胞转染后宫颈癌细胞株增殖和迁移能力的影响。通过免疫共沉淀 (Co-IP) 鉴定 KDM1A 与 HDAC1 的相互作用。通过qRT-PCR和蛋白质印迹测定宫颈癌细胞系中KDM1A和DACT1的表达水平。结果. TCGA数据库显示宫颈癌组织KDM1A表达升高，DACT1表达降低，与宫颈癌细胞系观察结果一致。发现 KDM1A 通过组蛋白去乙酰化负调节 DACT1。同时，KDM1A的下调或DACT1的过表达可以抑制HeLa和SiHa细胞的增殖和迁移能力。KDM1A 和 DACT1 过表达的共转染可以逆转由 KDM1A 过表达诱导的细胞增殖和迁移能力的增加。结论。KDM1A可以通过组蛋白去乙酰化下调DACT1的表达，从而抑制宫颈癌细胞的增殖和迁移。