Nuclear Focal Adhesion Kinase Protects against Cisplatin Stress in Ovarian Carcinoma

Cancer Res Commun. 2024 Dec 1;4(12):3165-3179. doi: 10.1158/2767-9764.CRC-24-0382.

Abstract

FAK inhibitors are in combinatorial clinical testing with agents that prevent Ras-Raf-MAPK pathway activation in various cancers. This study suggests that nuclear FAK limits ERK/MAPK activation in supporting HGSOC cell survival to cisplatin stress. Overall, it is likely that targets of FAK-mediated survival signaling may be tumor type- and context-dependent.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antineoplastic Agents / pharmacology
  • Antineoplastic Agents / therapeutic use
  • Cell Line, Tumor
  • Cell Nucleus / drug effects
  • Cell Nucleus / metabolism
  • Cell Survival / drug effects
  • Cisplatin* / pharmacology
  • Female
  • Focal Adhesion Kinase 1* / metabolism
  • Focal Adhesion Protein-Tyrosine Kinases / antagonists & inhibitors
  • Focal Adhesion Protein-Tyrosine Kinases / metabolism
  • Humans
  • MAP Kinase Signaling System / drug effects
  • Ovarian Neoplasms* / drug therapy
  • Ovarian Neoplasms* / pathology

Substances

  • Cisplatin
  • Focal Adhesion Kinase 1
  • PTK2 protein, human
  • Antineoplastic Agents
  • Focal Adhesion Protein-Tyrosine Kinases