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miR-23b/SP1/c-myc forms a feed-forward loop supporting multiple myeloma cell growth.

M Fulciniti1, N Amodio2, R L Bandi1

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Blood Cancer Journal
|January 16, 2016
PubMed
Summary
This summary is machine-generated.

A novel c-Myc/miR-23b/Sp1 network drives cancer cell growth. Downregulation of microRNA-23b (miR-23b) in multiple myeloma and Waldenstrom's macroglobulinemia promotes cancer survival by activating Sp1 signaling.

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Area of Science:

  • Oncology
  • Molecular Biology
  • Gene Regulation

Background:

  • MicroRNA (miR) and transcription factor (TF) networks are crucial in cancer development.
  • Dysregulated networks are a hallmark of hematologic malignancies like multiple myeloma (MM) and Waldenstrom's macroglobulinemia (WM).

Purpose of the Study:

  • To elucidate a novel c-Myc/miR-23b/Sp1 feed-forward loop in MM and WM.
  • To investigate the role of miR-23b in MM and WM cell growth and survival.

Main Methods:

  • Analysis of miR-23b expression in MM and WM cells.
  • Gain-of-function studies using miR-23b mimics and stable cell lines.
  • Luciferase reporter assays to confirm Sp1 targeting.
  • Western blotting and caspase activity assays.

Main Results:

  • miR-23b was downregulated in MM and WM cells, particularly within the bone marrow milieu.
  • miR-23b functions as a tumor suppressor, inhibiting cell proliferation and survival and inducing apoptosis.
  • miR-23b directly targets Sp1, reducing Sp1-driven nuclear factor-κB activity.
  • c-Myc transcriptionally represses miR-23b, establishing a feed-forward loop.

Conclusions:

  • A novel c-Myc/miR-23b/Sp1 feed-forward loop critically regulates MM and WM cell growth and survival.
  • Repression of miR-23b by c-Myc promotes oncogenic Sp1 signaling, contributing to disease progression.