Long noncoding RNAs in hepatitis B virus replication and oncogenesis

Figure 3 Regulatory mechanisms of various long noncoding RNAs in hepatitis B virus replication and oncogenesis[2]. A: HOX transcript antisense RNA (HOTAIR), high expression in hepatocellular carcinoma, urothelial carcinoma associated 1 (UCA1), HOTAIR, LINC00152, PVT1, and antisense noncoding RNA in the INK4 locus (ANRIL) could regulate gene expression through epigenetic silencing; B: HOXA transcript at the distal tip, LINC00152, and metastasis associated in lung adenocarcinoma transcript 1 (MALAT1) could increase the expression of their target genes through transcriptional control; C: MALAT1 could modulate alternative splicing; D: Unigene56159, highly upregulated in liver cancer (HULC), hepatitis B virus (HBV) X protein-long interspersed nuclear elements 1, UCA1, ANRIL, LINC01149 variant, LINC01352, F11-AS1, LINC01232, n335586, XIST, SNHG5, SSTR5-AS1, and TRERNA1 regulate the gene expression through molecular sponging to sequester miRNAs; E: Long noncoding RNAs (lncRNAs) Ftx could produce miRNAs to regulate their target genes; F: LncRNA-Dreh and HULC could modulate protein stability; G: LncRNA HBVPTPAP could encode a small polypeptide to exert its function.