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Regulation and function of microRNA-152 in various types of cancers: its upstream regulators and downstream targets

Sara Jafarzadeh1, Abdollah Jafarzadeh2,3, Raziyeh Zandvakili4

  • 1Faculty of Medicine, Kerman University of Medical Sciences, Kerman, Iran.

Clinical and Experimental Medicine
|July 11, 2025
PubMed

Insights

MicroRNA-152 (miR-152) is a tumor suppressor frequently lost in many cancers due to epigenetic silencing. Restoring miR-152 shows promise for cancer therapy by targeting oncogenic pathways and overcoming chemoresistance.

Area of Science:

  • Molecular Biology
  • Epigenetics
  • Cancer Research

Background:

  • MicroRNAs (miRNAs) regulate gene expression by binding to mRNA targets.
  • MicroRNA-152 (miR-152) is often downregulated in various cancers, including breast, endometrial, and gastrointestinal malignancies.
  • This downregulation is primarily caused by promoter hypermethylation, a form of epigenetic silencing.

Purpose of the Study:

  • To review the upstream regulators and downstream targets of miR-152.
  • To explore the dual role of miR-152 in different cancer types.
  • To summarize the therapeutic potential of restoring miR-152 expression in oncology.

Main Methods:

  • Literature review of studies on miR-152 function and regulation in cancer.
  • Analysis of epigenetic mechanisms, including DNA methylation and sponging by noncoding RNAs.
  • Examination of preclinical therapeutic strategies involving miR-152 restoration.

Main Results:

  • miR-152 acts as a tumor suppressor by inhibiting oncogenic pathways like PI3K/AKT/mTOR and EMT.
  • Epigenetic silencing via DNMT1 and sponging by lncRNAs/circRNAs contribute to miR-152 downregulation.
  • miR-152 exhibits context-dependent roles, acting as an oncogene in some cancers like prostate cancer.
  • Restoration of miR-152 demonstrates therapeutic potential against chemoresistance and metastasis in preclinical models.

Conclusions:

  • miR-152 is a critical tumor suppressor with complex regulatory networks.
  • Its downregulation through epigenetic mechanisms is a key event in cancer progression.
  • Targeting miR-152 pathways offers a promising avenue for precision oncology treatments.
Keywords:
CancersMiR-152MicroRNA-152Noncoding RNAs

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