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Myc/Max dependent intronic long antisense noncoding RNA, EVA1A-AS, suppresses the expression of Myc/Max dependent anti-proliferating gene EVA1A in a U2 dependent manner

Sci Rep.. 2019; 
Niehus SE1, Allister AB1, Hoffmann A2, Wiehlmann L3, Tamura T1, Tran DDH4.
Products/Services Used Details Operation
Gene Synthesis Promoter regions of EVA1 (−1–478) and EVA1A-AS (−1–988) were cloned into pGL2-basic vector. pcDNA3.1+/C-(K)-DYK-MYC was purchased from Genscript (NJ,USA). Get A Quote

摘要

The Myc gene has been implicated in the pathogenesis of most types of human cancerous tumors. Myc/Max activates large numbers of pro-tumor genes; however it also induces anti-proliferation genes. When anti-proliferation genes are activated by Myc, cancer cells can only survive if they are downregulated. Hepatocellular carcinoma (HCC) specific intronic long noncoding antisense (lnc-AS) RNA, the EVA1A-AS gene, is located within the second intron (I2) of the EVA1A gene (EVA-1 homolog A) that encodes an anti-proliferation factor. Indeed, EVA1A, but not EVA1A-AS, is expressed in normal liver. Depletion of EVA1A-AS suppressed cell proliferation of HepG2 cells by upregulation of EVA1A. Overexpression of EVA1A caused c... More

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