Department of Gynecology, Huai'an First People's Hospital, Nanjing Medical University, Huai'an, P.R. China.
Department of Orthopedics, Huai'an First People's Hospital, Nanjing Medical University, Huai'an, P.R. China.
Oncol Res. 2018 Mar 5;26(2):241-247. doi: 10.3727/096504017X14953948675412. Epub 2017 May 21.
Epithelial ovarian cancer (EOC) is the one of most common gynecological malignant tumors with high mortality. A series of long noncoding RNAs (lncRNAs) have been validated to play a vital role in EOC tumorigenesis. Colon cancer-associated transcript 2 (CCAT2) has been verified as an oncogenic lncRNA in multiple tumors; however, the role of CCAT2 in EOC genesis is still unclear. The purpose of the present study was to probe the function of CCAT2 on EOC. Preliminary experiments found that CCAT2 expression was significantly upregulated in EOC tissues and cell lines compared to noncancerous tissue and cells. CCAT2 knockdown induced by interfering oligonucleotides could inhibit proliferation and promote apoptosis and induce cell cycle arrest at the G0/G1 phase. Bioinformatics analysis predicted that miR-424 targeted CCAT2, which was confirmed by luciferase reporter assay. Moreover, the miR-424 inhibitor rescued the tumorigenesis inhibition induced by CCAT2 knockdown. In summary, our findings illustrate that CCAT2 acts as competing endogenous RNA (ceRNA) or sponge via negatively targeting miR-424, providing a novel diagnostic marker and therapeutic target for EOC.
上皮性卵巢癌 (EOC) 是最常见的妇科恶性肿瘤之一，死亡率较高。一系列长链非编码 RNA (lncRNA) 已被证实在 EOC 肿瘤发生中发挥重要作用。结肠癌相关转录物 2 (CCAT2) 已被证实为多种肿瘤中的致癌 lncRNA；然而，CCAT2 在 EOC 发生中的作用尚不清楚。本研究旨在探讨 CCAT2 在 EOC 中的作用。初步实验发现，与非癌组织和细胞相比，EOC 组织和细胞系中 CCAT2 的表达明显上调。干扰寡核苷酸诱导的 CCAT2 敲低可抑制增殖，促进凋亡，并诱导细胞周期停滞在 G0/G1 期。生物信息学分析预测 miR-424 靶向 CCAT2，这通过荧光素酶报告基因检测得到证实。此外，miR-424 抑制剂挽救了 CCAT2 敲低引起的肿瘤发生抑制。总之，我们的研究结果表明，CCAT2 通过负向靶向 miR-424 作为竞争内源性 RNA (ceRNA) 或海绵，为 EOC 提供了一种新的诊断标志物和治疗靶点。
