Center Laboratory, Jinshan Hospital, Fudan University, Shanghai 201508, P.R. China.
Oncol Rep. 2018 Jun;39(6):2644-2652. doi: 10.3892/or.2018.6384. Epub 2018 Apr 19.
Epithelial ovarian cancer (EOC) is one of the most lethal malignancies of the female reproductive organs. Increasing evidence has revealed that long non‑coding RNAs (lncRNAs) participate in tumorigenesis. Metastasis associated lung adenocarcinoma transcript 1 (MALAT1) is an lncRNA and plays a role in various types of tumors. However, the function of MALAT1 on cellular behavior in EOC remains unclear. The current study explored the expression of MALAT1 in ovarian cancer tissues and in EOC cell lines. Quantitative RT‑PCR analysis revealed that the expression of MALAT1 was higher in human ovarian malignant tumor tissues and EOC cells than in normal ovarian tissues and non‑tumorous human ovarian surface epithelial cells, respectively. By analyzing the online database Kaplan‑Meier Plotter, MALAT1 was identified to be correlated with the overall survival (OS) and progression‑free survival (PFS) of patients with ovarian cancer. Furthermore, knockdown of MALAT1 by small interfering RNA (siRNA) significantly decreased EOC cell viability, migration, and invasion. Finally, dual‑luciferase reporter assays demonstrated that MALAT1 interacted with miR‑143‑3p, a miRNA that plays a role in EOC as demonstrated in our previous study. Inhibition of MALAT1 resulted in an increase of miR‑143‑3p expression, leading to a decrease of CMPK protein expression. In conclusion, our results indicated that MALAT1 was overexpressed in EOC. Silencing of MALAT1 decreased EOC cell viability and inhibited EOC cell migration and invasion. These data revealed that MALAT1 may serve as a new therapeutic target of human EOC.
上皮性卵巢癌(EOC)是女性生殖系统最致命的恶性肿瘤之一。越来越多的证据表明,长链非编码 RNA(lncRNA)参与了肿瘤的发生。转移相关肺腺癌转录物 1(MALAT1)是一种 lncRNA,在各种类型的肿瘤中发挥作用。然而,MALAT1 在上皮性卵巢癌细胞中的作用尚不清楚。本研究探讨了 MALAT1 在卵巢癌组织和 EOC 细胞系中的表达。定量 RT-PCR 分析显示,MALAT1 在人卵巢恶性肿瘤组织和 EOC 细胞中的表达均高于正常卵巢组织和非肿瘤性人卵巢表面上皮细胞。通过分析在线数据库 Kaplan-Meier Plotter,发现 MALAT1 与卵巢癌患者的总生存(OS)和无进展生存(PFS)相关。此外,通过小干扰 RNA(siRNA)敲低 MALAT1 显著降低了 EOC 细胞的活力、迁移和侵袭能力。最后,双荧光素酶报告基因实验表明,MALAT1 与 miR-143-3p 相互作用,miR-143-3p 是我们之前研究中证明在 EOC 中发挥作用的 miRNA。抑制 MALAT1 导致 miR-143-3p 表达增加,从而导致 CMPK 蛋白表达减少。综上所述,我们的结果表明 MALAT1 在 EOC 中过表达。沉默 MALAT1 可降低 EOC 细胞活力并抑制 EOC 细胞迁移和侵袭。这些数据表明,MALAT1 可能成为人类 EOC 的一个新的治疗靶点。