The role of LncRNA FAM83H-AS1 as an oncogenic factor in endometrial carcinoma and its associated signaling network

SONG Xiao-xia; JIANG Qiu-hui; ZHOU Xiao-li; LIU Xiao-yan; WANG Qian-qian; ZHAO Xiao-li

doi:10.13820/j.cnki.gdyx.20232587

Abstract：Objective To investigate the expression and signaling network of LncRNA FAM83 H-AS1 in endom-etrial carcinoma(EC).Methods Cancer tissues and adjacent tissues from 82 patients with esophageal cancer(EC)were collected for detection of the expression levels of FAM83H-AS1.The diagnostic value of FAM83H-AS1 in EC was analyzed by ROC curve,and the correlation between FAM83H-AS1 and clinical pathological data of EC patients was also analyzed.Long non-coding RNA(LncRNA)SNP sites were used to construct an LncRNA-miRNA interaction network.The GEPIA website was used to predict the co-expressed genes of FAM83H-AS1,and KEGG enrichment analysis was conducted to determine the pathways enriched in co-expressed genes of FAM83H-AS1.The correlations between FAM83H-AS1,patient prognosis,and immunity was predicted.The expression of FAM83H-AS1 in EC cells was inter-vened,and cell proliferation activity was detected using the Cell Counting Kit-8(CCK-8)method,while cell invasion was assessed using Transwell.Results Compared with adjacent tissues,FAM83H-AS1 expression was enhanced in cancer tissues(P＜0.05),and FAM83H-AS1 could serve as an effective molecular marker for EC diagnosis(AUC=0.841,P＜0.01).The expression of FAM83H-AS1 was related to the clinical staging and depth of muscle invasion in EC patients(both P＜0.05).Multiple miRNAs and mRNAs were found to be associated with FAM83H-AS1,and the co-expressed genes of FAM83H-AS1 were mainly enriched in pathways such as the cell cycle,endocytosis,and RNA degradation.UALCAN website predicted that patients with high expression of FAM83H-AS1 had a poorer prognosis,and Timer website predicted that the expression of FAM83H-AS1 was associated with CD8+T cells and macrophages.Com-pared with the Blank group,overexpression of FAM83H-AS1 promoted the proliferation and invasion of EC cells,while knockdown of FAM83H-AS1 inhibited the proliferation and invasion of EC cells(all P＜0.05).Conclusion FAM83H-AS1 may be a carcinogenic driver in EC and could serve as a potential therapeutic target for treating EC.