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BRAF activates and physically interacts with PAK to regulate cell motility.

Samantha K McCarty1, Motoyasu Saji1, Xiaoli Zhang1

  • 1Division of EndocrinologyDiabetes and Metabolism, Department of Internal MedicineDepartment of Molecular VirologyImmunology, and Medical GeneticsCenter for BiostatisticsThe Ohio State University and Arthur G. James Comprehensive Cancer Center, 565 McCampbell Hall, 1581 Dodd Dr., Columbus, Ohio 43210, USA.

Endocrine-Related Cancer
|September 18, 2014
PubMed
Summary
This summary is machine-generated.

BRAF kinase activates p21-activated kinase (PAK) signaling, promoting papillary thyroid cancer (PTC) cell motility. This BRAF-PAK interaction is crucial for tumor invasion and presents a potential therapeutic target in aggressive PTC.

Keywords:
BRAFPAK1cancer biologycell motilitythyroid cancer

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Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Signaling

Background:

  • Papillary thyroid cancers (PTCs) exhibit increased p21-activated kinase (PAK) signaling at invasive fronts.
  • Thyroid cancer cell motility is dependent on group 1 PAKs, especially PAK1.

Purpose of the Study:

  • To investigate the hypothesis that BRAF regulates thyroid cancer cell motility via PAK activation.
  • To elucidate the functional relationship between BRAF and PAK signaling in PTC.

Main Methods:

  • Utilized human thyroid cancer cell lines with BRAF knockdown and MEK inhibition.
  • Employed immunofluorescence and immunoprecipitation to study BRAF-PAK interactions.
  • Assessed cell migration and PAK phosphorylation.
  • Induced BRAFV600E expression in vivo in murine thyroid glands.

Main Results:

  • BRAF knockdown reduced PAK phosphorylation, while MEK inhibition did not affect PAK activity.
  • BRAF loss-induced inhibition of cell migration was rescued by active MEK1 or PAK1 overexpression.
  • BRAF and PAK1 were shown to co-localize, physically interact, and enhance interaction during mitosis.
  • In vivo induction of BRAFV600E increased PAK expression and activity.

Conclusions:

  • BRAF directly activates PAK signaling and physically interacts with PAK in thyroid cancer cells.
  • The BRAF-PAK pathway is a key regulator of thyroid cancer cell motility and invasion.
  • This signaling axis represents a potential therapeutic target for aggressive PTC.