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NFATc3 controls tumour growth by regulating proliferation and migration of human astroglioma cells

Katia Urso1, Andrés Fernández2, Patricia Velasco3

  • 1Department of Vascular Biology and Inflammation, Centro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, Spain.

Scientific Reports
|June 29, 2019
PubMed

Insights

The Calcium/Calcineurin/Nuclear Factor of Activated T cells (Ca/CN/NFAT) pathway, specifically NFATc3, is crucial for glioma cell biology. Silencing NFATc3 inhibits tumor growth, proliferation, and migration, suggesting it as a potential therapeutic target.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Oncology

Background:

  • The Calcium/Calcineurin/Nuclear Factor of Activated T cells (Ca/CN/NFAT) pathway regulates calcium-dependent signaling in brain tissue homeostasis.
  • Aberrant signaling pathways are implicated in the pathogenesis of human gliomas.

Purpose of the Study:

  • To investigate the role of NFATc members in human glioma.
  • To determine the specific NFATc member predominantly expressed in glioma cells.
  • To elucidate the function of NFATc3 in glioma biology and its potential as a therapeutic target.

Main Methods:

  • Analysis of NFATc member expression in U251 and primary human glioblastoma (hGB) cell lines.
  • Utilized constitutive active NFATc3 mutant and shRNA lentiviral vectors for gene silencing.
  • Investigated cytokine and molecule regulation by the NFATc3 pathway.
  • Performed orthotopic intracranial assays with U251 cells.
  • Assessed in vitro proliferation and migration capacities of glioma cells.

Main Results:

  • NFATc3 was identified as the predominant NFATc member in human glioma cells.
  • Specific silencing of NFATc3 altered the expression of regulated cytokines and molecules essential for cancer cell biology.
  • NFATc3 silencing significantly inhibited tumor growth in an orthotopic intracranial assay.
  • Knock-down of NFATc3 reduced glioma cell proliferation and migration in vitro.

Conclusions:

  • NFATc3 plays a critical role in the proliferation, migration, and tumor growth of human glioma.
  • Targeting the NFATc3 pathway presents a promising therapeutic strategy for glioma treatment.

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