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Myc/Max dependent long antisense noncoding RNA, EVA1A-AS, participates in survival of hepatocellular carcinoma (HCC) by suppressing anti proliferating gene Eva1A.

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE115139 | GEO | 2019/12/10

REPOSITORIES: GEO

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Project description:Chronic infections by hepatitis B virus (HBV) and hepatitis C virus (HCV) appear to be the most significant causes of hepatocellular carcinoma (HCC). Aberrant promoter methylation is known to be deeply involved in cancer, including HCC. In this study, we analyzed aberrant promoter methylation on genome-wide scale in 6 HCCs including 3 HBV-related and 3 HCV-related HCCs, 6 matched noncancerous liver tissues and 3 normal liver tissues by methylated DNA immunoprecipitation-on-chip analysis. Candidate genes with promoter methylation were detected more frequently in HCV-related HCC. Candidate genes methylated preferentially to HBV-related or HCV-related HCCs were detected and selected, and methylation levels of the selected genes were validated using 125 liver tissue samples, including 61 HCCs (28 HBV-related HCCs and 33 HCV-related HCCs) and matched 59 matched noncancerous livers, and 5 normal livers, by quantitative methylation analysis using MALDI-TOF mass spectrometry. Among analyzed genes, preferential methylation in HBV-related HCC was validated in 1 gene only. However, 15 genes were found methylated preferentially in HCV-related HCC, which was independent from age. Hierarchical clustering of HCC using these 15 genes stratified HCV-related HCC as a cluster of frequently methylated samples. The 15 genes included genes inhibitory to cancer-related signaling such as RAS/RAF/ERK and Wnt/b-catenin pathways. It was indicated that genes methylated preferentially in HCV-related HCC exist, and it was suggested that DNA methylation might play an important role in HCV-related HCC by silencing cancer-related pathway inhibitors. we analyzed aberrant promoter methylation in 6 HCC clinical samples (including 3 HBV-related HCCs and 3 HCV-related HCCs) and their matched noncancerous tissues on genome-wide scale by the method. Candidate regions of promoter methylation preferentially to HBV-related HCC and HCV-related HCC were selected, and the methylation levels of these genes were measured quantitatively using MALDI-TOF mass spectrometry. Expression levels of these 6 pairs of HCC and 4 more pairs of HCCs and surrounding noncancerous tissues were analyzed by expression array and are reported in this Series. <br><br>This experiment was reloaded in November 2010 after additional curation. this dataset is part of the TransQST collection.

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Myc/Max dependent long antisense noncoding RNA, EVA1A-AS, participates in survival of hepatocellular carcinoma (HCC) by suppressing anti proliferating gene Eva1A.

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