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Altered Calcium Influx Pathways in Cancer-Associated Fibroblasts.

Francisco Sadras1, Teneale A Stewart2, Mélanie Robitaille1

  • 1School of Pharmacy, The University of Queensland, Brisbane, QLD 4102, Australia.

Biomedicines
|July 2, 2021
PubMed
Summary

Cancer-associated fibroblasts (CAFs) are key to tumor growth. Targeting specific calcium channels (VGCCs) like CaV1.2 and CaV3.2 offers a new therapeutic strategy for breast cancer by inhibiting CAF activation.

Keywords:
breast cancercalciumcalcium signallingcancer-associated fibroblastsstore-operated calcium entryvoltage-gated calcium channels

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Area of Science:

  • Cell Biology
  • Cancer Biology
  • Molecular Medicine

Background:

  • Cancer-associated fibroblasts (CAFs) are crucial components of the tumor microenvironment, influencing disease progression.
  • The role of calcium signaling pathways in CAF phenotype induction was previously unexplored.
  • Calcium signaling is recognized for its involvement in tumorigenesis.

Purpose of the Study:

  • To investigate the role of calcium signaling pathways in the induction of the CAF phenotype.
  • To explore the potential of targeting calcium signaling for therapeutic intervention in breast CAFs.

Main Methods:

  • Generated a CAF model (HMF3S-CAF) using transforming growth factor beta 1 (TGFβ1) stimulation.
  • Assessed functional changes in calcium signaling using fluorescent indicators, gene expression, gene silencing (siRNA), and pharmacological inhibition.
  • Investigated the expression of voltage-gated calcium channels (VGCCs) in CAFs.

Main Results:

  • HMF3S-CAF cells exhibited altered calcium influx pathways, notably reduced store-operated calcium entry.
  • Two VGCCs, CaV1.2 and CaV3.2, were upregulated in both the HMF3S-CAF model and patient-derived breast CAFs.
  • Silencing or pharmacological inhibition of CaV1.2 and CaV3.2 significantly impaired CAF activation.

Conclusions:

  • VGCCs play a role in TGFβ1-mediated induction of CAFs.
  • Targeting CaV1.2 and CaV3.2 through transcriptional interference or pharmacological antagonism inhibits CAF induction.
  • Targeting calcium signaling presents a potential therapeutic strategy for breast CAFs.