Long noncoding RNA ROR1-AS1 enhances STC2-mediated cell growth and autophagy in cervical cancer through miR-670-3p

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.

Keywords:

• Cervical cancer
• ROR1-AS1
• miR-670-3p
• STC2

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Correction

Acknowledgements

The authors highly appreciated all the labor members involved in this research.

Disclosure statement

The authors report no declarations of interest.