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The bromodomain inhibitor JQ1 up-regulates the long non-coding RNA MALAT1 in cultured human hepatic carcinoma cells

Hae In Choi1, Ga Yeong An1, Eunyoung Yoo1

  • 1Department of Bionanotechnology, Hanyang University, Seoul, 04673, Republic of Korea.

Scientific Reports
|May 13, 2022
PubMed

Insights

Bromodomain-containing 4 (BRD4) inhibition affects hepatocellular carcinoma (HCC) by altering MALAT1 lncRNA expression. Targeting FOXA2 may enhance BET inhibitor anti-cancer therapy efficacy.

Area of Science:

  • Molecular Biology
  • Epigenetics
  • Cancer Research

Background:

  • Bromodomain-containing 4 (BRD4) is overexpressed in hepatocellular carcinoma (HCC).
  • BRD4 inhibition is a potential therapeutic strategy for HCC.
  • Long non-coding RNAs (lncRNAs) are implicated in BRD4 inhibitor effects, but mechanisms are unclear.

Purpose of the Study:

  • To investigate the molecular mechanisms of JQ1, a BRD4 inhibitor, in HCC cells.
  • To characterize the regulation of MALAT1 by BRD4 and FOXA2.
  • To explore potential therapeutic targets for HCC.

Main Methods:

  • Gene network analysis
  • Chromatin immunoprecipitation sequencing (ChIP-seq) and quantitative PCR (ChIP-qPCR)
  • Luciferase reporter assays
  • Chromatin conformation capture (3C)
  • Cell proliferation assays

Main Results:

  • JQ1 treatment altered chromatin looping at the MALAT1 locus, involving enhancers (E1, E2, E3), gene body, and promoter.
  • JQ1 reduced proliferation-related lncRNAs but upregulated MALAT1.
  • Forkhead box protein A2 (FOXA2) binds to MALAT1 enhancer E2 and promoter.
  • FOXA2 suppression led to MALAT1 upregulation and increased cell proliferation.

Conclusions:

  • BRD4 inhibition impacts HCC via MALAT1 regulation.
  • Targeting FOXA2 may offer a therapeutic strategy to enhance anti-cancer effects.
  • MALAT1 inhibition could improve BET inhibitor efficacy in HCC treatment.

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