Ovarian cancer is one of the leading lethal gynecological cancers, causing serious harm to the health of female populations. Growing studies emphasize that lncRNAs serve as significant regulators in the tumorigenesis and evolution of numerous malignancies, including ovarian cancer. Recently, the oncogenic activity of lncRNA ARAP1-AS1 has been justified in a variety of cancers. However, the potential function of ARAP1-AS1 in ovarian cancer development is still unclear. Herein, we firstly revealed the expression profile of ARAP1-AS1 in ovarian cancer. Compared to normal samples and cells, upregulation of ARAP1-AS1 was observed in tissues and cells of ovarian cancer. Therewith, it was disclosed that knockdown of ARAP1-AS1 alleviated the carcinogenicity of ovarian cancer cells. Besides, our findings delineated that ARAP1-AS1 silence inhibited the expression of oncogene PLAGL2. Considering that ARAP1-AS1 was principally expressed in the the cytoplasm of ovarian cancer cells, we speculated that ARAP1-AS1 facilitated ovarian cancer progression via functioning as a ceRNA. Further investigations indicated that ARAP1-AS1 promoted PLAGL2 expression by competitively binding with miR-4735-3p. Of note, ARAP1-AS1 contributed to the malignant phenotypes of ovarian cancer cells through modulation of miR-4735-3p/PLAGL2 axis, revealing ARAP1-AS1 as a promising therapeutic target for ovarian cancer patients.

卵巢癌是最主要的致命妇科癌症之一，对女性人群的健康造成严重危害。越来越多的研究强调，lncRNA 在包括卵巢癌在内的多种恶性肿瘤的肿瘤发生和进化中起着重要的调节作用。最近，lncRNA ARAP1-AS1 的致癌活性已在多种癌症中得到证实。然而，ARAP1-AS1 在卵巢癌发展中的潜在功能仍不清楚。在此，我们首次揭示了 ARAP1-AS1 在卵巢癌中的表达谱。与正常样本和细胞相比，在卵巢癌的组织和细胞中观察到 ARAP1-AS1 的上调。因此，公开了ARAP1-AS1的敲低减轻了卵巢癌细胞的致癌性。除了，我们的研究结果表明 ARAP1-AS1 沉默抑制了癌基因 PLAGL2 的表达。考虑到 ARAP1-AS1 主要在卵巢癌细胞的细胞质中表达，我们推测 ARAP1-AS1 通过充当 ceRNA 促进卵巢癌的进展。进一步的研究表明，ARAP1-AS1 通过与 miR-4735-3p 竞争性结合来促进 PLAGL2 的表达。值得注意的是，ARAP1-AS1 通过调节 miR-4735-3p/PLAGL2 轴促进卵巢癌细胞的恶性表型，揭示了 ARAP1-AS1 作为卵巢癌患者有希望的治疗靶点。进一步的研究表明，ARAP1-AS1 通过与 miR-4735-3p 竞争性结合来促进 PLAGL2 的表达。值得注意的是，ARAP1-AS1 通过调节 miR-4735-3p/PLAGL2 轴促进卵巢癌细胞的恶性表型，揭示了 ARAP1-AS1 作为卵巢癌患者有希望的治疗靶点。进一步的研究表明，ARAP1-AS1 通过与 miR-4735-3p 竞争性结合来促进 PLAGL2 的表达。值得注意的是，ARAP1-AS1 通过调节 miR-4735-3p/PLAGL2 轴促进卵巢癌细胞的恶性表型，揭示了 ARAP1-AS1 作为卵巢癌患者有希望的治疗靶点。