Objectives Over the past years, growing attention has been paid to deciphering the pivotal role of long non‐coding RNAs (lncRNAs) in regulating the occurrence and development of human malignancies, cervical cancer (CC) included. Nonetheless, the regulatory role of lncRNA BBOX1 antisense RNA 1 (BBOX1‐AS1) has not been explored as yet. Material and Methods The expression of BBOX1‐AS1 was detected by reverse transcription real‐time quantitative polymerase chain reaction (RT‐qPCR). Cell Counting Kit‐8 (CCK‐8), colony formation, TUNEL, Western blot, transwell and immunofluorescence assays testified the critical role of BBOX1‐AS1 in CC. The relationship between RNAs (BBOX1‐AS1, miR‐361‐3p, HOXC6 and HuR) was analysed by luciferase reporter, RNA Immunoprecipitation (RIP) and RNA pull‐down assays. Results BBOX1 antisense RNA 1 antisense RNA 1 was revealed to be highly expressed in CC. Decreased expression of BBOX1‐AS1 had suppressive effects on CC cell growth and migration. Molecular mechanism assays verified that BBOX1‐AS1 had negative interaction with miR‐361‐3p in CC. Additionally, homeobox C6 (HOXC6) was validated to be a downstream target of miR‐361‐3p in CC. Furthermore, ELAV‐like RNA‐binding protein 1, also known as HuR, was uncovered to be capable of regulating the mRNA stability of HOXC6 in CC. More importantly, rescue assays delineated that knockdown of HuR after overexpressing miR‐361‐3p could reverse BBOX1‐AS1 upregulation‐mediated effect on CC progression. Similarly, the function induced by BBOX1‐AS1 upregulation on CC progression could be countervailed by HOXC6 depletion. Conclusions BBOX1 antisense RNA 1 facilitates CC progression by upregulating HOXC6 expression via miR‐361‐3p and HuR.

Accepted as a malignant tumor worldwide, cervical cancer (CC) has attracted much attention for its high incidence and mortality rates. Previous studies have elucidated the critical regulatory function that long noncoding RNAs (lncRNAs) exert on the tumorigenesis and progression of diverse tumors. Although multiple investigations have depicted that LINC00958 has a great impact on the complex biological process of many cancers, knowledge concerning the regulatory role of LINC00958 in CC remains limited and needs to be further explored. In our study, LINC00958 expression was evidently overexpressed in CC tissues and cells. Besides this, LINC00958 negatively regulated miR‐625‐5p expression and was verified to bind with miR‐625‐5p in CC. Subsequently, it was testified by a series of experiments that LINC00958 promotes CC cell proliferation and metastasis by sponging miR‐625‐5p. Furthermore, the leucine‐rich repeat containing the eight family member E (LRRC8E) could bind with miR‐625‐5p, and its expression was negatively modulated by miR‐625‐5p, whereas positively regulated by LINC00958 in CC. Final rescue assays verified the effects of LINC0095/LRRC8E interaction and miR‐625‐5p/LRRC8E interaction on CC cell proliferation and metastasis. Collectively, LINC00958 facilitates CC cell proliferation and metastasis via the miR‐625‐5p/LRRC8E axis.

Background: Previous literature has revealed long non-coding RNAs (lncRNAs) are crucial regulators for cell functions and gene expression. LncRNA fetal-lethal non-coding developmental regulatory RNA (FENDRR) was reported as a biological suppressor in several types of human cancers, yet relevant mechanisms and biological effects of FENDRR with regards to cervical cancer (CC) are not explored until now. Methods: In this study, quantitative real-time polymerase chain reaction (qRT-PCR) analysis detected gene expression in tissues and cells. Gain-or loss-of-function experiments revealed the biological effects of FENDRR and miR-15a/b-5p on CC cell functions. Bioinformatics tools were used to predict the relevant genes. Mechanism experiments including RNA immunoprecipitation (RIP) assay, pull down assay and luciferase reporter assay depicted the binding situation and coexistence of indicated genes. Results: FENDRR was downregulated in CC tissues and cells, which suppressed CC progression. MiR-15a-5p and miR-15b-5p shared binding sites with FENDRR and had interaction with FENDRR. Tubulin alpha1A (TUBA1A) was downregulated in CC tissues and positively modulated by FENDRR. TUBA1A was the target of miR-15a/b-5p. TUBA1A silencing rescued the effect of FENDRR overexpression on CC cell growth and migration. Conclusion: FENDRR inhibits CC progression through upregulating TUBA1A in a miR-15a/b-5p-dependent manner.