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Genome-wide Screen for miRNA Targets Using the MISSION Target ID Library
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MicroRNA-21 targets Sprouty2 and promotes cellular outgrowths

Danish Sayed1, Shweta Rane, Jacqueline Lypowy

  • 1Cardiovascular Research Institute, Department of Cell Biology and Molecular Medicine, University of Medicine and Dentistry of New Jersey, Newark, NJ 07103, USA.

Molecular Biology of the Cell
|May 30, 2008
PubMed

Insights

MicroRNA-21 (miR-21) promotes cell connections and protrusions in heart cells by downregulating Sprouty2 (SPRY2). This mechanism also impacts cancer cell migration and protrusions.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Cardiology

Background:

  • MicroRNA-21 (miR-21) is implicated in cancer and cardiac hypertrophy.
  • The precise function of miR-21 in cardiocytes and cancer remains to be fully elucidated.

Purpose of the Study:

  • To investigate the role of miR-21 in cardiocyte structure and function.
  • To explore the downstream targets and mechanisms of miR-21 in both cardiac and cancer cells.

Main Methods:

  • Overexpression and knockdown of miR-21 and Sprouty2 (SPRY2) in cultured cardiocytes and colon cancer cells.
  • Analysis of cellular morphology, including cell-to-cell connections and protrusions.
  • Investigation of beta-adrenergic receptor (betaAR) stimulation effects.

Main Results:

  • miR-21 overexpression in cardiocytes induced cell-to-cell outgrowths and branches.
  • miR-21 directly targets and down-regulates SPRY2, an inhibitor of branching.
  • betaAR stimulation up-regulated miR-21, down-regulated SPRY2, and promoted cellular connections.
  • SPRY2 knockdown mimicked miR-21's branching effect, while miR-21 knockdown or SPRY2 overexpression inhibited it.
  • In colon cancer cells, miR-21 knockdown reduced microvillus-like protrusions and inhibited migration in a SPRY2-dependent manner.

Conclusions:

  • miR-21 promotes the formation of cellular protrusions and connections by targeting SPRY2.
  • This mechanism is conserved in both cardiac cells and cancer cells, influencing cell migration.

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