Nuclear Focal Adhesion Kinase Protects against Cisplatin Stress in Ovarian Carcinoma

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...

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Bibliographic Details
Published in:Cancer research communications 2024-12, Vol.4 (12), p.3165
Main Authors: Zhang, Yichi, Ojalill, Marjaana, Boyer, Antonia, Chen, Xiao Lei, Tahon, Elise, Thivolle Lioux, Gaëtan, Xia, Marvin, Abbas, Maryam, Soylu, Halime Meryem, Flieder, Douglas B, Connolly, Denise C, Molinolo, Alfredo A, McHale, Michael T, Stupack, Dwayne G, Schlaepfer, David D
Format: Article
Language:English
Subjects:
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
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Summary: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.
ISSN:2767-9764
2767-9764
DOI:10.1158/2767-9764.CRC-24-0382