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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Veröffentlicht in:	Cancer research communications 2024-12, Vol.4 (12), p.3165-3179
Hauptverfasser:	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:	Artikel
Sprache:	eng
Schlagworte:	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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Zusammenfassung:	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