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A decreasing function describes a relationship where the output consistently declines as the input increases. This means that for any two input values, if one is greater than the other, the corresponding output is smaller. Mathematically, a function f is decreasing on an interval I if for every x1 < x2​ in I, f (x1) > f (x2). This type of behavior is visually identified on a graph that slopes downward from left to right.The nature of a function can be analyzed by calculating...
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Overexpression of miR-133 decrease primary endothelial cells proliferation and migration via FGFR1 targeting.

Mina Soufi Zomorrod1, Fatemeh Kouhkan2, Masoud Soleimani1

  • 1Department of Hematology and Cell Therapy, Faculty of Medical Science, Tarbiat Modares University, Tehran, lran.

Experimental Cell Research
|April 3, 2018
PubMed
Summary
This summary is machine-generated.

MicroRNA-133 (miR-133) inhibits tumor angiogenesis by targeting FGFR1 signaling in endothelial cells. This finding offers a potential therapeutic strategy to block cancer growth by suppressing new blood vessel formation.

Keywords:
AngiogenesisCancerFGFR1miR-133

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Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Angiogenesis, the formation of new blood vessels, is a critical process in tumor growth and metastasis.
  • Fibroblast Growth Factor Receptor 1 (FGFR1) signaling is essential for endothelial cell (EC) functions, including proliferation, migration, and tube formation, which are vital for angiogenesis.
  • The balance of positive and negative regulators controls angiogenesis, making it a key target for cancer therapies.

Purpose of the Study:

  • To investigate the regulatory role of microRNA-133 (miR-133) in FGFR1 expression.
  • To determine if miR-133 modulates basic Fibroblast Growth Factor (bFGF)/FGFR1 activity in ECs.
  • To explore the potential of targeting FGFR1 by miR-133 to inhibit tumor angiogenesis.

Main Methods:

  • Overexpression of miR-133 in endothelial cells stimulated with bFGF.
  • Assessment of EC proliferation using cell growth curves and MTT assays.
  • Evaluation of EC migration and capillary-like tube formation.
  • Quantification of FGFR1 mRNA and protein levels in transfected ECs.

Main Results:

  • Forced expression of miR-133 significantly reduced bFGF-induced EC proliferation and migration.
  • miR-133 expression showed a negative correlation with both mRNA and protein levels of FGFR1.
  • Overexpression of miR-133 disrupted capillary network formation and reduced cell division rates in ECs.

Conclusions:

  • MiR-133 plays a significant role in regulating bFGF-induced angiogenesis in endothelial cells.
  • Targeting FGFR1 with miR-133 presents a promising therapeutic strategy for suppressing tumor angiogenesis and cancer progression.