Coupling docetaxel with NOS inhibition increased EnR-stress response via coactivation of ATF4 and CHOP, which triggered the pASK1/JNK proapoptotic pathway, promoting cleavage of caspases 3 and 9.<b>Conclusions:</b> iNOS is a critical target for docetaxel resistance in TNBC.
We defined an eight-gene signature with prognostic potential, altered in 45% of 2,509 patients with breast cancer.<b>Conclusions:</b> ATF4 may represent a valuable prognostic biomarker and therapeutic target in patients with TNBC, and we identified a cell signaling pathway-based gene signature that may contribute to the development of combinatorial targeted therapies for breast cancer.<i></i>.