Fig. 5

SE-associated lncRNA in tumors. Red rectangles represent SEs, black rectangles represent lncRNA, acute-angle arrows represent facilitation, and right-angle arrows represent repression in the figure. (A)SE-lncRNAs are involved in transcriptional regulation and chromatin interactions in cancer. SE-LINC00162 inhibits the transcription of PTTG1IP, hence reducing the expression of PTTG1IP and promoting the proliferation of bladder cancer cells. SE-CCAT1-L, located within a SE and close to MYC, promotes long-range chromatin looping in human colorectal cancers. (B)SE-lncRNAs form a positive feedback loop with TFs in cancer. HCCL5 is overexpressed in human HCC tissues and is regulated by ZEB1 transcription through a SE, while increased HCCL5 exacerbates the EMT phenotype by inducing ZEB1 expression, which creates positive feedback. LncRNA DSCAM-AS1 can interact with YBX1, controls the expression of FOXA1, and advances breast cancer. FOXA1-driven SEs can also transcribe and activate lncRNA DSCAM-AS1 to create a positive feedback loop. (C)SE-lncRNAs act as competing endogenous or Sponging RNAs in cancer. In non-small cell lung cancer samples, SE-lncRNA LINC01503 may competitively bind LASP1 with miR-342-3p. MIR205HG depletes endogenous miR-590-3p leading to increased YAP, cdk1, and cyclin B protein expression in Head and Neck Squamous Cell Carcinoma. (D)SE-lncRNAs are involved in signal transduction pathways in cancer. LncRNA UCA1 expression is positively correlated with SEs and has been identified as a regulator of the Hippo-YAP signaling pathway, highlighting the role of the UCA1-AMOT-YAP signaling axis in ovarian cancer progression. (BLC = Bladder cancer, BRC = Breast cancer, CRC = colorectal cancer, ESCC = esophageal squamous cell carcinoma, HCC = Hepatocellular carcinoma, NSCLC = Non-small cell lung cancer, SCC = Squamous cell carcinoma, OC = Ovarian cancer.)