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Updated: Mar 8, 2026

Investigation of the Transcriptional Role of a RUNX1 Intronic Silencer by CRISPR/Cas9 Ribonucleoprotein in Acute Myeloid Leukemia Cells
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Investigation of the Transcriptional Role of a RUNX1 Intronic Silencer by CRISPR/Cas9 Ribonucleoprotein in Acute Myeloid Leukemia Cells

Published on: September 1, 2019

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RUNX3 is oncogenic in natural killer/T-cell lymphoma and is transcriptionally regulated by MYC

V Selvarajan1, M Osato2,3, G S S Nah2

  • 1Department of Pathology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore.

Leukemia
|January 26, 2017
PubMed

Insights

RUNX3 is overexpressed in natural killer/T-cell lymphoma (NKTL), promoting cancer growth. MYC drives this RUNX3 upregulation, suggesting MYC inhibition as a potential NKTL therapy.

Area of Science:

  • Molecular Biology
  • Oncology
  • Immunology

Background:

  • RUNX3 (runt-domain transcription factor) is a key gene regulator with context-dependent roles in cancer.
  • Natural killer/T-cell lymphoma (NKTL) is an aggressive lymphoid malignancy.
  • RUNX3's specific role in NKTL pathogenesis is not well understood.

Purpose of the Study:

  • To investigate the role of RUNX3 in NKTL.
  • To identify upstream regulators of RUNX3 in NKTL.
  • To explore therapeutic strategies targeting the RUNX3 pathway in NKTL.

Main Methods:

  • Quantitative PCR and Western blotting to assess RUNX3 expression in NKTL samples and cell lines.
  • RNA interference to silence RUNX3 and assess its impact on NKTL cell apoptosis and proliferation.
  • Chromatin immunoprecipitation assays to investigate MYC binding to the RUNX3 enhancer.
  • Reporter assays to confirm MYC-driven RUNX3 transcription.
  • Treatment of NKTL cells with the MYC inhibitor JQ1 and assessment of cell viability and apoptosis.

Main Results:

  • RUNX3 mRNA and protein are significantly upregulated in NKTL compared to normal NK cells.
  • RUNX3 silencing in NKTL cells increases apoptosis and reduces proliferation.
  • MYC binds to the RUNX3 enhancer region and positively regulates its transcription.
  • MYC inhibition using JQ1 downregulates both MYC and RUNX3, inducing apoptosis in NKTL cells.
  • Ectopic MYC expression rescues growth inhibition caused by MYC depletion.

Conclusions:

  • RUNX3 is oncogenic in NKTL and its overexpression contributes to tumor progression.
  • MYC is a key upstream regulator of RUNX3 in NKTL.
  • Targeting MYC, potentially through inhibition, represents a promising therapeutic avenue for NKTL.

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