Abstract

Purpose

Cervical cancer (CC) ranks the fourth among female malignancies and has become a dominating cause for tumor-associated death nowadays. More and more documents have proposed that long noncoding RNAs (lncRNAs), which emerge as pivotal biomarkers, actively participate in the regulation of human carcinomas. LncRNA ROR1-AS1 is a recently identified RNA that is highlighted for its crucial role in the biological processes of cancers. However, the role and molecular mechanism of ROR1-AS1 in CC have not been clarified yet.

Methods and results

In the current study, RT-qPCR analysis uncovered that ROR1-AS1 expression was evidently upregulated in CC tissues and cell lines. Functional experiments (CCK-8, EdU, TUNEL, wound healing and Transwell assays as well as western blot analysis) revealed that knockdown of ROR1-AS1 markedly suppressed the malignant phenotypes of CC cells via decreasing cell viability, proliferation, migration, invasion and autography, and facilitating cell apoptosis. Subsequently, by performing luciferase reporter and RNA pulldown assays, miR-670-3p was identified to be sponged by ROR1-AS1. Additionally, STC2 was disclosed to be targeted by miR-670-3p in CC cells. Rescue assays illuminated that upregulation of STC2 counteracted ROR1-AS1 knockdown-induced suppression on CC cell growth.

Conclusions

These data suggested that ROR1-AS1 contributed to the malignant properties of CC cells through sponging miR-670-3p and upregulating of STC2.

中文翻译：

---

长链非编码 RNA ROR1-AS1 通过 miR-670-3p 增强 STC2 介导的宫颈癌细胞生长和自噬

摘要

目的

宫颈癌（CC）在女性恶性肿瘤中排名第四，已成为当今肿瘤相关死亡的主要原因。越来越多的文献提出，作为关键生物标志物出现的长链非编码 RNA (lncRNA) 积极参与人类癌症的调控。LncRNA ROR1-AS1 是最近发现的一种 RNA，因其在癌症生物学过程中的关键作用而备受关注。然而，ROR1-AS1在CC中的作用和分子机制尚未阐明。

方法和结果

在目前的研究中，RT-qPCR 分析发现 ROR1-AS1 表达在 CC 组织和细胞系中明显上调。功能实验（CCK-8、EdU、TUNEL、伤口愈合和 Transwell 检测以及蛋白质印迹分析）表明，ROR1-AS1 的敲低通过降低细胞活力、增殖、迁移、侵袭和自显影显着抑制 CC 细胞的恶性表型，并促进细胞凋亡。随后，通过进行荧光素酶报告基因和 RNA 下拉分析，确定 miR-670-3p 被 ROR1-AS1 吸收。此外，STC2 被披露为在 CC 细胞中被 miR-670-3p 靶向。救援分析表明 STC2 的上调抵消了 ROR1-AS1 敲低诱导的对 CC 细胞生长的抑制。

结论

这些数据表明，ROR1-AS1 通过海绵化 miR-670-3p 和上调 STC2 促进了 CC 细胞的恶性特性。