HDAC1 functions as an oncogene in multi-type cancers. This study aimed to investigate the roles of histone deacetylase 1 (HDAC1) in cervical cancer (CC). mRNA expression was determined using reverse transcription quantitative polymerase chain reaction. The protein−protein complexes was analyzed using co-immunoprecipitation assay. The binding sites between NRF2 and NEU1 were confirmed by chromatin immunoprecipitation assay. Cell viability was detected by CCK-8. Cell proliferation was measured using CCK-8 and colony formation assays. Cell migrative and invasive ability were determined using transwell assay. We found that HDAC1 was upregulated in CC patients and cells. Trichostatin A (TSA) treatment decreased the number of colonies and migrated and invaded cells. Moreover, HDAC1 interacted with NRF2 to downregulate NEU1 expression. NEU1 knockdown attenuated the effects of TSA and enhanced the aggressiveness of CC cells. In conclusion, HDAC1 functions as an oncogene in CC. Targeting HDAC1 may be an alternative strategy for CC.

中文翻译：

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HDAC1 介导的 NEU1 下调加剧了宫颈癌的侵袭性

HDAC1 在多种癌症中充当癌基因。本研究旨在探讨组蛋白脱乙酰酶 1 (HDAC1) 在宫颈癌 (CC) 中的作用。使用逆转录定量聚合酶链反应测定mRNA表达。使用免疫共沉淀分析对蛋白质-蛋白质复合物进行分析。通过染色质免疫沉淀测定证实了 NRF2 和 NEU1 之间的结合位点。通过CCK-8检测细胞活力。使用 CCK-8 和集落形成测定来测量细胞增殖。使用transwell测定测定细胞的迁移和侵袭能力。我们发现 HDAC1 在 CC 患者和细胞中表达上调。曲古抑素 A (TSA) 处理减少了集落数量以及迁移和侵袭细胞的数量。此外，HDAC1 与 NRF2 相互作用，下调 NEU1 表达。 NEU1 敲低减弱了 TSA 的作用并增强了 CC 细胞的侵袭性。总之，HDAC1 在 CC 中充当癌基因。针对 HDAC1 可能是 CC 的替代策略。