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Induction and Analysis of Epithelial to Mesenchymal Transition
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Calcium signaling induces a partial EMT.

Robert J Norgard1, Jason R Pitarresi1, Ravikanth Maddipati2

  • 1Abramson Family Cancer Research Institute and Department of Medicine, University of Pennsylvania, Philadelphia, PA, USA.

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|July 29, 2021
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Prolonged calcium signaling triggers partial epithelial-to-mesenchymal transition (P-EMT) in carcinoma cells. This cellular plasticity enhances tumor cell invasion and migration, posing challenges for cancer therapy.

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Area of Science:

  • Oncology
  • Cell Biology
  • Cancer Research

Background:

  • Epithelial plasticity, specifically epithelial-to-mesenchymal transition (EMT), grants tumor cells invasive capabilities, complicating cancer treatment.
  • Carcinoma cells exist on a spectrum of hybrid epithelial-mesenchymal (E-M) states, with partial EMT (P-EMT) states exhibiting higher metastatic potential.

Purpose of the Study:

  • To investigate the mechanisms underlying partial epithelial-to-mesenchymal transition (P-EMT) in carcinoma cells.
  • To identify signaling pathways that induce P-EMT and enhance cellular invasion.

Main Methods:

  • Induction of P-EMT through prolonged calcium signaling.
  • Analysis of E-cadherin (ECAD) internalization and epithelial protein localization.
  • Investigating signaling pathways involving Gαq-associated G-protein-coupled receptors (GPCRs) and calmodulin-Camk2b.

Main Results:

  • Prolonged calcium signaling induced P-EMT, characterized by E-cadherin internalization and increased cell migration and invasion.
  • Signaling via Gαq-coupled GPCRs mimicked these P-EMT effects.
  • Downstream activation of calmodulin-Camk2b signaling was identified as a key mechanism.

Conclusions:

  • Calcium signaling acts as a critical trigger for the acquisition of hybrid/partial epithelial-mesenchymal states in carcinoma cells.
  • Understanding these mechanisms offers potential therapeutic targets for inhibiting cancer metastasis.