Abstract
Ovarian cancer is one of the most common female reproductive system malignancies worldwide. Recently, the aberrant long noncoding RNAs (lncRNAs) expression has been identified in multiple cancers. Emerging evidence has highlighted the critical roles of lncRNAs in carcinogenesis and tumor progression, including ovarian cancer. The objective of this study is to comprehensively analyze lncRNAs expression pattern, and explore their clinical significance and underlying mechanism in human ovarian cancer. In this study, we found hundreds of dysregulated lncRNAs in ovarian cancer by performing genome‐wide analysis using RNA sequencing data from Genotype‐Tissue Expression (GTEx) and The Cancer Genome Atlas (TCGA) project, and three microarray datasets from Gene Expression Omnibus (GEO). Moreover, our results revealed that up‐ or down‐regulation of some lncRNAs expression in ovarian cancer is accompanied by their genomic loci copy number amplification or deletion. Importantly, some lncRNAs expression levels are significantly associated with ovarian cancer patients’ poor prognosis. Further experimental validation and mechanistic investigation indicate that LINC00511 exerts oncogenic function in ovarian cancer cells through interacting with EZH2 and repressing P21 expression. Taken together, the findings in the current study may provide a useful resource of novel ovarian cancer associated lncRNAs and potential diagnostic biomarker and therapeutic targets for ovarian cancer.
Highlights
Ovarian carcinoma is one of the most common reproductive system malignancies in female residents, and has been one of the leading causes of cancer‐related death worldwide.[1]
Benefit from the rapid development of high‐throughput techniques, a variety of cancer genomics projects have been implemented to identify genomic, epigenomic, and transcrip tomic alterations and determine different molecular pathways in human cancers. These investigations have focused on long noncoding RNAs (lncRNAs) as well as protein‐coding genes, which have been found to be a significant regulator for a diverse of biological processes.[26]
Yan et al reported that lncRNA MLK7‐AS1 was up‐regulated in ovar ian cancer tissues and cell lines, and promoted cell prolif eration, migration and invasion through binding to miR‐375 and thereby reversing its inhibitory effect on regulating the Yes‐associated protein 1 (YAP1) expression in ovarian can cer.[27]
Summary
Ovarian carcinoma is one of the most common reproductive system malignancies in female residents, and has been one of the leading causes of cancer‐related death worldwide.[1]. A growing number of evidence has been revealed that lots of the noncoding regions in human genome are actively transcribed.[6,7] Further sequencing and annota tion of these transcripts leads to the discovery of thousands of long noncoding RNAs (lncRNAs), which is longer than 200 nt in length and lacking of protein coding capacity.[8,9] In addition, emerging studies indicate that lncRNAs are key regulators involved in almost every aspect of intracellular biological process, including the chromatin remodeling, X chromatin imprinting, cell differentiation and fate decision, immune response, tumor cells growth and metastasis etc.[10,11] Importantly, lncRNAs dysregulation have been reported in diverse human disease, especially cancers.[13] Accumulating evidence reveals that lncRNAs exert their roles in tumori genesis and tumor progression by repressing tumor suppres sors or activating oncogenes through multiple mechanisms, including acting as cancer‐related microRNAs sponges, re cruiting histone modifiers to target genes and regulating their transcription, affecting mRNA decay and translation.[14,15] For instance, Sun and colleagues reported that lncRNA HOXA11‐AS promoted gastric cancer tumorigenesis through functioning as scaffold of chromatin modification factors LSD1, PRC2, and DNMT1.16 In addition, lncRNA PDCD4‐ AS1 contributes to breast cancer progression by stabilizing PDCD4 mRNA through forming RNA duplex and controlling PDCD4 mRNA’s interaction with RNA decay promoting fac tor HuR.[17] LINC01234 promotes the malignancy of gastric cancer via acting as a competing endogenous RNA for miR‐204‐5p to regulate CBFB expression.[18]
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