宫颈癌（CC）仍然是全球女性癌症相关死亡的主要原因。长非编码 RNA (lncRNA) 在包括 CC 在内的多种癌症中发挥着至关重要的调节作用。本研究探讨了一种新型 lncRNA USP30 反义 RNA 1 (USP30-AS1) 在 CC 肿瘤发生中的功能。我们使用 RT-qPCR 分析了 USP30-AS1 的表达，并进行了体外功能丧失测定以及体内测定，以评估 USP30-AS1 沉默对 CC 细胞生长和迁移的影响。进行了其他机制实验，包括 RNA Pull-down、RNA 免疫沉淀 (RIP) 和免疫共沉淀 (Co-IP) 测定，以阐明 USP30-AS1 影响的调节机制。我们发现 USP30-AS1 在 CC 组织和细胞中过度表达。沉默USP30-AS1可显着减少细胞增殖、迁移、侵袭和肿瘤生长。此外，发现 USP30-AS1 通过海绵 microRNA-2467-3p (miR-2467-3p) 并招募 FUS RNA 结合蛋白 (FUS) 来调节泛素特异性肽酶 30 (USP30) 的表达，从而稳定 β-catenin并激活 Wnt/β-catenin 信号通路。这些研究结果表明，USP30-AS1 通过 miR-2467-3p/FUS/USP30 轴增强 CC 细胞生长和迁移，突显其作为 CC 生物标志物的潜力。© 2024 Wiley‐VCH GmbH。

Cervical cancer (CC) remains a major cause of cancer-related mortality among women globally. Long noncoding RNAs (lncRNAs) play crucial regulatory roles in various cancers, including CC. This study investigates the function of a novel lncRNA, USP30 antisense RNA 1 (USP30-AS1), in CC tumorigenesis. We analyzed USP30-AS1 expression using RT-qPCR and conducted in vitro loss-of-function assays, as well as in vivo assays, to evaluate the effects of USP30-AS1 silencing on CC cell growth and migration. Additional mechanistic experiments, including RNA pull-down, RNA immunoprecipitation (RIP), and co-immunoprecipitation (Co-IP) assays, were performed to elucidate the regulatory mechanisms influenced by USP30-AS1. We discovered that USP30-AS1 is overexpressed in CC tissues and cells. Silencing USP30-AS1 significantly reduced cell proliferation, migration, invasion, and tumor growth. Moreover, USP30-AS1 was found to modulate the expression of ubiquitin-specific peptidase 30 (USP30) by sponging microRNA-2467-3p (miR-2467-3p) and recruiting the FUS RNA binding protein (FUS), thereby stabilizing β-catenin and activating the Wnt/β-catenin signaling pathway. These findings suggest that USP30-AS1 enhances CC cell growth and migration through the miR-2467-3p/FUS/USP30 axis, highlighting its potential as a biomarker for CC.© 2024 Wiley‐VCH GmbH.