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Anti-miR-17 therapy delays tumorigenesis in MYC-driven hepatocellular carcinoma (HCC)

Renumathy Dhanasekaran1,2,3, Meital Gabay-Ryan2,3, Virginie Baylot2,3

  • 1Division of Gastroenterology and Hepatology, Department of Medicine, Stanford University School of Medicine, Stanford, CA, USA.

Oncotarget
|February 22, 2018
PubMed

Insights

Targeting microRNAs regulated by MYC, such as miR-17, offers a new therapeutic strategy for hepatocellular carcinoma (HCC). Blocking miR-17 in MYC-driven HCC mouse models significantly delayed tumor growth by reducing proliferation and increasing apoptosis.

Area of Science:

  • Oncology
  • Molecular Biology
  • Gene Therapy

Background:

  • Hepatocellular carcinoma (HCC) presents a major clinical challenge with limited treatment options.
  • MYC oncogene amplification/overexpression is frequent in HCC, making it a therapeutic target.
  • Direct MYC-targeting drugs are unavailable; targeting downstream microRNAs is an alternative.

Purpose of the Study:

  • To investigate the therapeutic potential of blocking miR-17, a MYC-regulated microRNA, in a mouse model of MYC-driven HCC.
  • To evaluate the efficacy of systemic delivery of anti-miR-17 using lipid nanoparticles (LNPs).

Main Methods:

  • Utilized a conditional transgenic mouse model of MYC-driven HCC.
  • Administered systemic anti-miR-17 oligonucleotide encapsulated in LNPs.
  • Performed global gene expression profiling to assess target engagement and pathway modulation.

Main Results:

  • Anti-miR-17 treatment de-repressed miR-17 direct targets, induced significant apoptosis, and decreased proliferation in vivo.
  • Tumorigenesis was significantly delayed in MYC-driven HCC mouse models treated with anti-miR-17.
  • Gene expression analysis confirmed engagement of miR-17 targets and inhibition of MYC-driven cell cycle and proliferation pathways.

Conclusions:

  • Systemic delivery of anti-miR-17 is an effective therapeutic strategy for MYC-driven HCC.
  • Targeting miR-17 offers a promising approach to inhibit MYC oncogenic activity in liver cancer.
Keywords:
HCCMYClipid nanoparticle (LNP)liver cancermiR

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