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Updated: May 20, 2026

RhoC GTPase Activation Assay
09:58

RhoC GTPase Activation Assay

Published on: August 22, 2010

BART inhibits pancreatic cancer cell invasion by Rac1 inactivation through direct binding to active Rac1

Keisuke Taniuchi1, Kunihiko Yokotani, Toshiji Saibara

  • 1Department of Pharmacology, School of Medicine, Kochi University, Nankoku, Kochi, Japan. ktaniuchi@kochi-u.ac.jp

Neoplasia (New York, N.Y.)
|June 30, 2012
PubMed

Insights

Binder of Arl Two (BART) inhibits pancreatic cancer cell invasion by regulating Rac1 activity. BART suppression increases Rac1 activity and cell invasion, while Rac1 inhibitors reduce invasiveness.

Area of Science:

  • Oncology
  • Cell Biology
  • Molecular Biology

Background:

  • Binder of Arl Two (BART) is a protein interacting with ADP-ribosylation factor-like 2, involved in microtubule dynamics.
  • The Rho GTPase protein Rac1 is implicated in cell migration and invasion processes.

Purpose of the Study:

  • To investigate the role of BART in regulating pancreatic cancer cell invasion.
  • To elucidate the mechanism by which BART affects cell invasion, focusing on its interaction with Rac1.

Main Methods:

  • Investigated BART's interaction with active Rac1 in pancreatic cancer cells.
  • Assessed the impact of BART suppression on Rac1 activity and cell invasion.
  • Utilized Rac1 inhibitors to evaluate their effect on invasiveness in BART-knockdown cells.
  • Observed actin-cytoskeleton rearrangements, including membrane ruffling and lamellipodia formation.

Main Results:

  • BART interacts with active Rac1 at the leading edges of migrating cancer cells.
  • Suppression of BART leads to increased active Rac1 and enhanced cell invasion.
  • Rac1 inhibition reduces invasiveness in pancreatic cancer cells with suppressed BART.
  • BART suppression induces membrane ruffling and lamellipodia formation, dependent on Rac1 activity.

Conclusions:

  • BART inhibits pancreatic cancer cell invasion by modulating Rac1 activity.
  • The BART-Rac1 complex regulates actin-cytoskeleton rearrangements crucial for invasion.
  • Targeting the BART-Rac1 pathway may offer therapeutic strategies for pancreatic cancer.

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