Significance The cJun NH2-terminal kinase (JNK) signaling pathway has been implicated in the etiology of breast cancer because mutations in the JNK pathway have been identified in tumors. To test… Click to show full abstract
Significance The cJun NH2-terminal kinase (JNK) signaling pathway has been implicated in the etiology of breast cancer because mutations in the JNK pathway have been identified in tumors. To test the role of the JNK pathway, we studied an in vitro CRISPR-based model of HER2+ cancer using human mammary epithelial cells and an in vivo mouse genetic model of HER2+ breast cancer. The data obtained demonstrated that JNK deficiency and HER2 signaling caused similar changes in gene expression in 3D cultures of human mammary epithelial cells in vitro. Moreover, JNK deficiency caused accelerated development of mouse breast cancer in vivo. These observations establish a tumor suppression function for the JNK signaling pathway in HER2+ breast cancer.
               
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