GSE115139
Myc/Max dependent long antisense noncoding RNA, EVA1A-AS, participates in survival of hepatocellular carcinoma (HCC) by suppressing anti proliferating gene Eva1A.
Cancer cells associated with multiple survival strategies, and how cancer cells escape cell death under different conditions are still largely unknown. The Myc gene has been implicated in the pathogenesis of most types of human tumors. We show here that Eva1 (eva-1homolog A)/TMEM166 (transmembrane protein 166)/family with sequence similarity 176 (FAM176A) is upregulated by Myc/Max, however, overexpression of Eva1A induced mitotic catastrophe in hepatocellular carcinoma (HCC).  Here, expression of Eva1A in HCC is suppressed by antisense long noncoding RNA, Eva1A-AS, that is induced also by Myc/Max, suggesting that Eva1A-AS expression supports HCC survival.  Eva1A-AS is located within intron of Eva1A gene suppressed Eva1 expression by forming double stranded RNA with DiGeorge syndrome chromosomal region 8 (DGCR8). Depletion of Eva1A-AS in HepG2 cells upregulates Eva1A expression, and induced accumulation of lipid droplets and stopped cell proliferation. Furthermore, suppressed Eva1A expression levels are negatively correlated with differentiation grade in 371 primary HCCs. These data also suggest that EVA1A-AS may be useful target for a subset of HCCs. Overall design: mRNA profile of shRNA control infected HepG2 and shTHOC5 infected were generated by deep sequencing.