Protein Kinase D Enzymes as Regulators of EMT and Cancer Cell Invasion

Nisha Durand1, Sahra Borges2, Peter Storz3

  • 1Department of Cancer Biology, Mayo Clinic, 4500 San Pablo Road, Jacksonville, FL 32224, USA. durand.nisha@mayo.edu.

Insights

Protein Kinase D (PKD) isoforms have distinct roles in cell migration and epithelial to mesenchymal transition (EMT). Understanding these roles is crucial, as dysregulated PKD expression is linked to cancer progression.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Oncology

Background:

  • Protein Kinase D (PKD) isoforms (PKD1, PKD2, PKD3) are downstream effectors of novel Protein Kinase Cs (nPKCs) and diacylglycerol (DAG).
  • PKDs regulate critical cellular functions including protein transport, cell migration, proliferation, epithelial to mesenchymal transition (EMT), and apoptosis.
  • Distinct roles of PKD isoforms in cellular processes are emerging, with PKD1 inhibiting EMT and cell migration, while PKD2 and PKD3 promote these processes.

Purpose of the Study:

  • To review the regulatory mechanisms of EMT and cell migration by PKD isoforms.
  • To elucidate the significance of PKD-mediated regulation in cancer development.

Main Methods:

  • Literature review focusing on studies investigating PKD isoforms, EMT, cell migration, and cancer.
  • Analysis of experimental data and findings from published research.

Main Results:

  • PKD isoforms exhibit differential regulation of EMT and cell migration.
  • PKD1 acts as an inhibitor of EMT and cell migration.
  • PKD2 and PKD3 function as promoters of EMT and cell migration.

Conclusions:

  • Aberrant expression of PKD isoforms is implicated in various cancers, including breast, pancreatic, and prostate cancer.
  • The distinct roles of PKD isoforms in EMT and cell migration highlight their importance in cancer initiation and progression.
  • Targeting PKD isoforms may offer therapeutic strategies for managing malignancies associated with altered EMT and cell migration.

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