The regulatory mechanisms of oncomiRs in cancer

Khalid Otmani1, Redouane Rouas1, Mimoune Berehab1

  • 1Hematology Laboratory, Hematology Department, Hôpital Universitaire de Bruxelles (H.U.B.) Institut Jules Bordet, Université Libre de Bruxelles, Brussels, Belgium.

Insights

This review explores how oncogenic microRNAs (oncomiRs) are upregulated in cancer. Understanding these epigenetic mechanisms is key to targeting oncomiRs for cancer therapy.

Area of Science:

  • Molecular Biology
  • Epigenetics
  • Cancer Research

Background:

  • Cancer arises from genetic alterations and epigenetic dysregulation affecting signaling pathways.
  • MicroRNAs (miRNAs) are key epigenetic regulators influencing tumor development.
  • miRNAs are classified as oncogenic (oncomiRs) or tumor suppressive (TS miRNAs) based on their targets.

Purpose of the Study:

  • To summarize mechanisms controlling the upregulation of oncomiRs in cancer cells and the tumor microenvironment (TME).
  • To highlight the role of non-transcriptional processes, like gene amplification, in oncomiR overexpression.
  • To provide insights into the critical role of oncomiRs in cancer development and progression.

Main Methods:

  • Review of existing literature on miRNA regulation in cancer.
  • Analysis of transcriptional, post-transcriptional, and non-transcriptional mechanisms.
  • Focus on oncomiR expression control in cancer cells and the TME.

Main Results:

  • OncomiR upregulation is driven by various regulatory mechanisms.
  • Transcriptional and post-transcriptional modifications are common, but non-transcriptional processes like gene amplification also contribute.
  • These mechanisms are active in both cancer cells and the surrounding tumor microenvironment.

Conclusions:

  • Detailed understanding of oncomiR upregulation mechanisms is crucial for cancer research.
  • Elucidating these pathways can reveal the critical role of oncomiRs in tumorigenesis.
  • This knowledge may facilitate the development of novel cancer therapeutic strategies targeting oncomiRs.

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