Objectives Cervical cancer is an aggressive malignant tumour and causes high mortality in women. LncRNA HOXA-AS2 is a tumour promoter in many cancers. The current work was designed to elucidate the functions of HOXA-AS2 in cervical cancer and the underlying regulatory mechanism. Methods qRT-PCR was conducted to reveal RNA levels. A FISH assay was conducted for the identification of the subcellular location of HOXA-AS2. MTT, EdU, Transwell and tube formation were used for detection of cell growth, migration and angiogenesis, respectively. In-vivo studies were conducted to reveal the role of HOXA-AS2 on transplanted tumour growth in mice. Key findings The HOXA-AS2 level was found high in tissues and cells of cervical cancer. Silencing of HOXA-AS2 restrained cell proliferation, migration and invasion. Angiogenesis of HUVECs was restrained after silencing HOXA-AS2. Additionally, HOXA-AS2 upregulated the BTN3A1 by interaction with miR-509-3p. BTN3A1 overexpression rescues the inhibitory effect of silenced HOXA-AS2 on cell phenotypes in cervical cancer. Moreover, xenograft tumour growth in mice was suppressed by HOXA-AS2 depletion and was facilitated by BTN3A1 overexpression. Conclusions HOXA-AS2 accelerates cellular progression in cervical cancer by the miR-509-3p/BTN3A1 axis.

Background: Cervical cancer, the leading cause of cancer-relevant mortality in females, is an aggressive malignant tumor. Tumor angiogenesis is vital for cell proliferation and metastasis in cancers. Accumulating studies have claimed that long non-coding RNAs (lncRNAs) participate in the progression of various cancers. The aim of this research is to explore the biological role and regulatory mechanism of LncRNA HOXA-AS2 in cervical cancer.Methods: Experiments including RT-qPCR, western blot, RIP, MTT, EdU, transwell, luciferase reporter, RIP, FISH, tube formation assays were applied to investigate the biological role and regulatory mechanism of LncRNA HOXA-AS2 in cervical cancer.Results: In current study, the results disclosed that HOXA-AS2 was notably upregulated in cervical cancer tissues and cell lines, and high HOXA-AS2 expression was strongly associated with poor prognosis of cervical cancer patients. Furthermore, HOXA-AS2 contributed to cell proliferation, migration, invasion and angiogenesis in cervical cancer. In addition, HOXA-AS2 absorbed miR-509-3p and miR-509-3p targeted BTN3A1 in cervical cancer. Besides, BTN3A1 overexpression partly rescued the inhibitory influence of HOXA-AS2 knockdown on cervical cancer progression and angiogenesis. Overall, HOXA-AS2 promoted cervical cancer progression and angiogenesis through sponging miR-509-3p to elevate BTN3A1 expression. Conclusions: In other words, this paper was the first to study the molecular regulatory mechanism of HOXA-AS2 in cervical cancer and certified that HOXA-AS2 accelerated progression and angiogenesis in cervical cancer by targeting miR-509-3p/BTN3A1 axis, which may become a beneficial therapeutic target for cervical cancer.