Hsa_circ_0101119 facilitates the progression of cervical cancer via an interaction with EIF4A3 to inhibit TCEAL6 expression.

Abstract

Recently, circular RNAs (circRNAs/circs) have attracted increased attention due to their regulatory role in a variety of cancer types. However, the role and molecular mechanisms of circRNAs in cervical cancer (CC) remain unknown. The present study aimed to investigate the function of hsa_ circ_0101119 on CC and its potential mechanisms. The differentially expressed circRNAs associated with CC were screened out using R software, according to the database of Gene Expression Omnibus (GEO). The expression levels of hsa_circ_0101119, eukaryotic initiation factor 4A-3 (EIF4A3) and transcription elongation factor A-like 6 (TCEAL6) in CC cells were detected via reverse transcription-quantitative (RT-q)PCR, and their expression levels in CC tissues were analyzed based on the database of GEO and the Cancer Genome Atlas. Moreover, the accurate functions of hsa_circ_0101119 and TCEAL6 on the proliferation, apoptosis, migration and invasion of SiHa and HeLa cells was examined using colony formation assay, 5-ethynyl-20-deoxyuridine incorporation assay, flow cytometry and Transwell assay. Next, the underlying mechanisms of hsa_circ_0101119 on CC progression were determined via bioinformatics analysis, RNA immunoprecipitation assay, RNA pull down assay, RT-qPCR and western blotting. It was found that hsa_circ_0101119 was highly expressed in CC tissues and cells, while TCEAL6 was lowly expressed. Knockdown of hsa_circ_0101119 or TCEAL6 overexpression significantly inhibited the proliferation, migration and invasion of SiHa and HeLa cells, but facilitated apoptosis. It was also demonstrated that hsa_circ_0101119 could recruit EIF4A3 to inhibit TCEAL6 expression in CC. Furthermore, knockdown of TCEAL6 could reverse the effects of silencing hsa_circ_0101119 on the proliferation, apoptosis, migration and invasion of HeLa cells. In conclusion, the present study revealed that hsa_circ_0101119 could facilitate cell proliferation, migration and invasion, and suppress apoptosis in CC via an interaction with EIF4A3 to inhibit TCEAL6 expression, which may provide a potential therapeutic target for CC treatment.