Neuromedin U contributes to radiation resistance in colorectal cancer via YAP/TAZ signaling activation.

Resistance to radiation therapy remains a treatment obstacle for patients with high‑risk colorectal cancer. Neuromedin U () has been identified as a potential predictor of the response to radiation therapy by RNA sequencing analysis of colorectal cancer tissues obtained from patients. However, the role of in colorectal cancer remains unknown. In order to investigate role of in colorectal cancer, expression was regulated using small interfering RNA or an ‑expression pCMV3 vector, and cell counting, wound‑healing and clonogenic assays were subsequently performed. knockdown decreased colorectal cancer cell proliferation and migration, and sensitized the cells to radiation. Conversely, overexpression increased radiation resistance, proliferation and migration of colorectal cancer cells. Furthermore, by western blotting and nuclear fractionation experiments, knockdown inhibited the nuclear translocation of yes‑associated protein (YAP) and transcriptional co‑activator with PDZ‑binding motif (TAZ), resulting from the phosphorylation of these proteins. By contrast, the nuclear translocation of YAP and TAZ was increased following overexpression in colorectal cancer cells. Recombinant regulated YAP and TAZ activity, and the expression of the YAP and TAZ transcriptional target genes , connective tissue growth factor and cysteine‑rich angiogenic inducer 61 in an NMU receptor 1 activity‑dependent manner. These results suggested that may contribute to the acquisition of radioresistance in colorectal cancer by enhancing the Hippo signaling pathway via YAP and TAZ activation.