NEK8 regulates colorectal cancer progression via phosphorylating MYC

Radiotherapy and chemotherapy remain the mainstay of treatment for colorectal cancer (CRC), although their efficacy is limited. A detailed understanding of the molecular mechanisms underlying CRC progression could lead to the development of new therapeutic strategies. Although it has been established that MYC signaling is dysregulated in various human cancers, direct targeting MYC remains challenging due to its undruggable protein structure. Post-translational modification of proteins can affect their stability, activation, and subcellular localization. Hence, targeting the post-translational modification of MYC represents a promising approach to disrupting MYC signaling. Herein, we revealed that NEK8 positively regulates CRC progression by phosphorylating c-MYC protein at serine 405, which exhibited enhanced stability via polyubiquitination. Our findings shed light on the role of NEK8/MYC signaling in CRC progression, offering a novel and helpful target for colorectal cancer treatment.

Automated summary

Radiotherapy and chemotherapy are the main treatment methods for colorectal cancer, but their effectiveness is limited. Understanding the molecular mechanisms of colorectal cancer progression could lead to the development of new therapies. NEK8 positively regulates CRC progression by phosphorylating c-MYC protein at serine 405, enhancing its stability through polyubiquitination. This study highlights the role of NEK8/MYC signaling as a potential target for colorectal cancer treatment.