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BART inhibits pancreatic cancer cell invasion by PKCα inactivation through binding to ANX7

Keisuke Taniuchi1, Kunihiko Yokotani, Toshiji Saibara

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

Plos One
|April 26, 2012
PubMed

Insights

Binder of Arl two (BART) and annexin7 (ANX7) act as anti-invasive molecules in pancreatic cancer. They regulate protein kinase C alpha (PKCα) activity, inhibiting cancer cell invasiveness.

Area of Science:

  • Molecular biology
  • Cancer research
  • Cell biology

Background:

  • Annexin7 (ANX7) exhibits tumor suppressor functions in human cancers.
  • ANX7 is a Ca(2+)-dependent, phosphorylated GTPase membrane fusion protein.
  • The role of ANX7 in pancreatic cancer invasiveness requires further elucidation.

Purpose of the Study:

  • To investigate the novel function of the binder of Arl two (BART) molecule in pancreatic cancer.
  • To elucidate the interaction between BART, ANX7, and protein kinase C alpha (PKCα) in regulating cancer cell invasion.

Main Methods:

  • Investigated the binding interaction between BART and ANX7.
  • Examined the effect of the BART-ANX7 complex on PKCα activity.
  • Utilized gene knockdown and pharmacological inhibitors to assess cell invasiveness.

Main Results:

  • BART inhibits pancreatic cancer cell invasiveness by binding to ANX7.
  • The BART-ANX7 complex is transported to cell protrusions in migrating cells.
  • BART binding to ANX7 reduces PKCα activity, thereby decreasing cancer cell invasiveness.

Conclusions:

  • BART and ANX7 function as anti-invasive molecules in pancreatic cancer.
  • The BART-ANX7 complex regulates PKCα activity and downstream signaling.
  • BART and ANX7 represent potential therapeutic targets for reducing pancreatic cancer cell invasion.

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