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FBXL5 attenuates RhoGDI2-induced cisplatin resistance in gastric cancer cells

W-D Wu1, M Wang, H-H Ding

  • 1Department of Gastrointestinal Surgery, and 2Department of Oncology; Shanghai General Hospital of Nanjing Medical University, Shanghai, China. Zheng_junQiu@126.com.

European Review for Medical and Pharmacological Sciences
|July 8, 2016
PubMed
Abstract

Insights

F-box and leucine-rich repeat protein 5 (FBXL5) interacts with Rho GDP dissociation inhibitor 2 (RhoGDI2), attenuating cisplatin resistance in gastric cancer. This suggests FBXL5 is a therapeutic target for gastric cancers with RhoGDI2-induced chemoresistance.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • F-box and leucine-rich repeat protein 5 (FBXL5) is an E3 ubiquitin ligase subunit involved in cancer metastasis and chemoresistance.
  • FBXL5 targets diverse substrates for ubiquitin-mediated degradation, regulating cellular processes.

Purpose of the Study:

  • To investigate the interaction between FBXL5 and Rho GDP dissociation inhibitor 2 (RhoGDI2).
  • To elucidate the role of FBXL5 in regulating cisplatin resistance and migration in gastric cancer cells.

Main Methods:

  • Immunoprecipitation (IP) coupled with mass spectrometry.
  • Analysis of FBXL5-RhoGDI2 interaction and its effect on gastric cancer cell chemoresistance and migration.
  • Assessment of Erk and p38 activation upon FBXL5 depletion.

Main Results:

  • FBXL5 interacts with RhoGDI2 and attenuates RhoGDI2-induced cisplatin resistance in gastric cancer cells.
  • FBXL5 regulates gastric cancer migration through cortactin degradation.
  • FBXL5 depletion enhances cisplatin resistance via Erk and p38 activation, while FBXL5 itself is degraded in response to cisplatin in RhoGDI2-overexpressing cells.

Conclusions:

  • A negative feedback loop exists between FBXL5 and RhoGDI2 in RhoGDI2-induced cisplatin resistance in gastric cancer.
  • FBXL5 represents a novel therapeutic target for gastric cancers exhibiting RhoGDI2-induced cisplatin resistance.

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