Abstract

Opa-interacting protein 5 antisense transcript 1 (OIP5-AS1) is one kind of cytoplasmic long non-coding RNA (lncRNA), which has been demonstrated to play a critical function in multiple cancers. However, the detailed mechanism of OIP5-AS1 in the regulation of cervical cancer progression is still obscure. Here, we demonstrated that lncRNA OIP5-AS1 was upregulated in cervical cancer and was correlated with poor prognosis by bioinformatics studies. OIP5-AS1 depletion inhibited cell proliferation and promoted cell apoptosis in cervical cancer cells. Furthermore, we clarified that ROCK1 was the downstream effector of OIP5-AS1 and OIP5-AS1 acted as a molecular sponge of miR-143-3p. Finally, we verified that OIP5-AS1 exerted its function in the regulation of cervical cancer progression via interacting with miR-143-3p to regulate ROCK1 expression. Our study revealed novel mechanisms about how lncRNA OIP5-AS1 executed its function in cervical cancer and thus provided potential therapeutic targets for the disease.

Highlights

  • Cervical cancer (CC) is one of the most common cancer types in women worldwide and a leading cause of tumor-related deaths among women globally [1,2]

  • Several long non-coding RNA (lncRNA) have been reported to be involved in the progression of CC. lncRNA TUSC8 plays an important role in inhibiting the invasion and migration of CC cells via miR641/PTEN axis [9]. lncRNA MIR205HG acts as a competing endogenous RNA and modulates tumor growth and progression via sponging miR-122-5p in CC [10]

  • Few researchers have reported the connection between lncRNA OIP5-AS1 and CC progression [2,30]

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Summary

Introduction

Cervical cancer (CC) is one of the most common cancer types in women worldwide and a leading cause of tumor-related deaths among women globally [1,2]. Long non-coding RNAs (lncRNAs) are RNAs with a length of more than 200 nucleotides and are not translated into proteins [4,5,6]. Their functional disorders and specific roles in various diseases, especially cancers, have attracted increasing attention [7,8]. LncRNA MIR205HG acts as a competing endogenous RNA (ceRNA) and modulates tumor growth and progression via sponging miR-122-5p in CC [10]. LncRNA HOST2 is demonstrated to be upregulated in HPV-positive CC and promote cell proliferation, migration, and invasion via sponging let-7b [11]. LncRNA GHET1 is reported to act as an oncogenic lncRNA in CC [13]

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