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Myc/Max dependent intronic long antisense noncoding RNA, EVA1A-AS, suppresses the expression of Myc/Max dependent

Svenja E Niehus1, Aldrige B Allister1, Andrea Hoffmann2

  • 1Institut fuer Biochemie, OE4310, Medizinische Hochschule Hannover, Carl-Neuberg-Str. 1, D-30623, Hannover, Germany.

Scientific Reports
|November 23, 2019
PubMed

Insights

The Myc gene drives cancer by activating both pro-tumor and anti-proliferation genes. In liver cancer (HCC), EVA1A-AS RNA controls the anti-proliferation gene EVA1A, crucial for cancer cell survival.

Area of Science:

  • Oncology
  • Molecular Biology
  • Gene Regulation

Background:

  • The Myc/Max complex plays a dual role in cancer, activating pro-tumor genes while also inducing anti-proliferation genes.
  • Hepatocellular carcinoma (HCC) survival depends on downregulating Myc-induced anti-proliferation genes.
  • EVA1A, an anti-proliferation factor, is encoded by the EVA1A gene, with its antisense long noncoding RNA (lnc-AS) EVA1A-AS located in its second intron.

Purpose of the Study:

  • To investigate the role of the EVA1A-AS lnc-AS RNA in hepatocellular carcinoma (HCC) pathogenesis.
  • To elucidate the regulatory relationship between EVA1A, EVA1A-AS, and the Myc/Max complex in HCC.

Main Methods:

  • Analysis of EVA1A and EVA1A-AS expression in HCC tissues and cell lines.
  • Gene depletion and overexpression studies in HepG2 cells.
  • Correlation analysis between gene expression levels, differentiation grade, and patient survival in HCC cohorts.

Main Results:

  • EVA1A-AS depletion upregulated EVA1A, suppressing HepG2 cell proliferation.
  • EVA1A overexpression induced G2/M phase cell death via microtubule catastrophe.
  • Suppressed EVA1A expression correlated with poor differentiation in HCC, while EVA1A-AS expression correlated with better patient survival.
  • Both EVA1A and EVA1A-AS were identified as Myc/Max targets.

Conclusions:

  • The Myc/Max complex regulates the anti-proliferation gene EVA1A and its antisense lnc-AS RNA EVA1A-AS in HCC.
  • EVA1A-AS acts as a crucial regulator for HCC cell survival by controlling EVA1A expression.
  • EVA1A-AS represents a potential therapeutic target for hepatocellular carcinoma.

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