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.
Original language | English |
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Pages (from-to) | 3165-3179 |
Number of pages | 15 |
Journal | Cancer Research Communications |
Volume | 4 |
Issue number | 12 |
Early online date | Nov 25 2024 |
DOIs | |
State | Published - Dec 1 2024 |
Keywords
- Antineoplastic Agents/pharmacology
- Cell Line, Tumor
- Cell Nucleus/drug effects
- Cell Survival/drug effects
- Cisplatin/pharmacology
- Female
- Focal Adhesion Kinase 1/metabolism
- Focal Adhesion Protein-Tyrosine Kinases/metabolism
- Humans
- MAP Kinase Signaling System/drug effects
- Ovarian Neoplasms/drug therapy