Fig. 2

LncRNAs network in malignant transformation of HCC stem cells. Part 1: LncRNA CUDR impacts the malignant proliferation of liver CSCs trough different pathways. LncRNA CUDR act as oncogene by CUDR-HULC/CUDR-β-catenin signaling pathway; CUDR inhibits the methylation of gene promoter LncRNA H19 by combining with Cyclin-D to form the complex CUDR-CyclinD1, which upregulates the expression of LncRNA H19 and finally upregulates the expression of TERT and C-Myc to promote self-renewal and proliferation of HCC stem cells; LncRNA CUDR facilitate the interaction between SET1A and phosphorylated RB1 (pRB1) to be a complex contributing to the high level of H3K4 trimethylation, which took part in the malignant transformation of HCC stem cells via altering the length of telomere. Part 2: LncRNA HOTAIR can inhibit histone H3K36 trimethylation by suppressing SETD2. Then, to enhance the malignant proliferation of HCC stem cells via affecting the repair of aged histone, microsatellite stability, and cell cycle-related genes. Part 3: LncRNA TCF7 alter the expression of TCF7 by recruiting complex SWI/SNF to combine with TCF7 promoter region, which could activate WNT signaling pathways and accelerate self-renewal of HCC stem cells. Part 4: LncRNA DILC can inhibit liver CSCs’ self-renewal through the IL-6/STAT3 signaling pathway