Long non-coding RNA FAM83H-AS1 acts as a potential oncogenic driver in human ovarian cancer

• Main Authors: Xiaolei Yuan (Author), Ying Huang (Author), Man Guo (Author), Xiaowei Hu (Author), Peiling Li (Author)
• Format: Book
• Published: BMC, 2021-01-01T00:00:00Z.
• Subjects: article
• Online Access: Connect to this object online.
• Notes: 10.1186/s13048-020-00756-y; 1757-2215
• Keywords: Ovarian cancer; lncRNA FAM83H-AS1; Network; Survival; Immune; Gynecology and obstetrics; RG1-991
• Source: Journal of Ovarian Research, Vol 14, Iss 1, Pp 1-10 (2021)

Abstract Objective Ovarian cancer (OC) is one of the most aggressive women cancers with increasing incidence and mortality rates worldwide. Long non-coding RNAs (lncRNAs) could as major players in OC process. Although FAM83H antisense RNA1 (FAM83H-AS1) is demonstrated play an important roles in a many cancers, the detailed function and mechanism has not been reported in OC. Results We integrated multiple kinds of bioinformatics approaches and experiments validated method to evaluate functions of FAM83H-AS1 in OC. Some differential expressed lncRNAs were identified between OC and normal control tissues. FAM83H-AS1 was one of most differentially expressed lncRNAs and up-regulated in multiple cancer types. Specially, expression of FAM83H-AS1 was higher in OC and showed difference in diverse stages. High FAM83H-AS1 expression is associated with worse pan-cancer and OC outcomes. FAM83H-AS1-centric network including lncRNA-miRNA, lncRNA-protein and lncRNA-mRNA ceRNA network were constructed to infer the function and mechanism of FAM83H-AS1. There were two methylation sites including cg01399317 and cg20519035 located at FAM83H-AS1. The methylation level of cg01399317 was correlated with gene expression of FAM83H-AS1. The expression level of FAM83H-AS1 was correlated with infiltration level of immune cell including macrophage, neutrphil and dendritic cell in OC patients. Lastly, qRT-PCR showed that the expression of FAM83H-AS1 was higher in OC tissues than normal control tissues. Conclusion Collectively, these results indicated that FAM83H-AS1 may act as an oncogenic driver and it may be a potential therapy target in OC.