Figure 4

Epigenomic analysis of OIP5-AS1 promoter and expression of associated lncRNAs. (a) Graphical view of OIP5-AS1 promoter region with regulatory elements binding, histone modification signatures in H1-hESC and immortalized undifferentiated chronic myelogenous leukemia cell line (K562) and position of MYC (red), NANOG (blue) and KLF4 (green) motifs present around 1 kb up and downstream from TSS. H3K4me3 and H3K27ac signature are strong in hESC and cancer cells suggesting its active role in maintaining stemness in stem cells and cancer cells. Further, FAIRE-Seq (Formaldehyde-Assisted Isolation of Regulatory Elements) displayed strong TF binding around the NANOG motif in hESC and MYC motif in cancer cells suggesting that the stemness regulatory pathways is facilitated by NANOG in hESC and MYC in cancer cells. (b) Sequences of MYC, NANOG and KLF4 motifs screened in the promoter sequence of OIP5-AS1. (c) Interaction network of OIP5-AS1 through bioinformatics screening showing OIP5-AS1 interacts with NEAT1, TUG1 and HOTAIR. (d) Expression levels of lncRNAs NEAT1, TUG1 and HOTAIR between OIP5-AS1 overexpressed and underexpressed oral tumors from this study. Statistical significance represented as ** for P < 0.01 and **** for P < 0.0001 (two-tailed Student’s t-test). (e) Correlation of expression between NEAT1, TUG1 and HOTAIR with OIP5-AS1. TUG1 and HOTAIR have a significant correlation in expression with OIP5-AS1.