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Background  Long non-coding RNA (lncRNA) plays an important role in tumorigenesis. The lncRNA  CCND2 AS1  has been shown to be involved in the growth of several tumors; however, its role in cervical cancer has not been elucidated. This study aimed to explore the expression, function, and underlying mechanism of action of  CCND2 AS1  in cervical cancer. Expression of  CCND2 AS1  was examined in cervical cancer and adjacent normal cervical tissues by quantitative real-time polymerase chain reaction (qRT-PCR) and by bioinformatic analysis of data from the Gene Expression Profiling Interactive Analysis (GEPIA) database. The function of  CCND2 AS1  was investigated by overexpressing or silencing  CCND2 AS1  in HeLa and SiHa cervical cancer cells followed by in vitro and in vivo analyses. Methylation-specific PCR (MSP) and bisulfite genomic sequencing (BGS) were used to detect  CCND2 AS1  promoter methylation status in cervical cancer cells.    Results   CCND2 AS1  expression was lower in cervical cancer compared with normal cervical tissues, and the level was significantly correlated with the patient age and tumor size.  CCND2 AS1  overexpression inhibited the proliferation and cell cycle progression of HeLa cells in vitro and/or in vivo, whereas  CCND2 AS1  silencing had the opposite effects.  CCND2 AS1  expression was elevated after treatment of cervical cancer cells with the DNA methyltransferase inhibitor 5′-azacytidine (5′-Aza), and this was mediated, at least in part, via reduced CpG methylation at the  CCND2 AS1  promoter.    Conclusion   CCND2 AS1  expression is downregulated in cervical cancer, potentially through increased  CCND2 AS1  promoter methylation, and the upregulation of  CCND2 AS1  expression inhibited tumor growth. These data suggest that  CCND2 AS1  could be a diagnostic marker and potential therapeutic target for cervical cancer.

Aberrant methylation-mediated downregulation of lncRNA CCND2 AS1 promotes cell proliferation in cervical cancer