Polo-Like Kinase 1 phosphorylates and stabilizes KLF4 to promote tumorigenesis in nasopharyngeal carcinoma

Conclusion: Our study unveiled a new PLK1-TRAF6-KLF4 feed-forward loop. The resulting increase in KLF4 ubiquitination leads to stabilization and upregulation of KLF4, which leads to tumorigenesis in NPC. These results expand our understanding of the role of KLF4 in NPC and validate PLK1 inhibitors as potential therapeutic agents for NPC, especially cancer patients with KLF4 overexpression.

Source: Theranostics - June 13, 2019 Category: Molecular Biology Authors: Jia Mai, Zhuo-Yan Zhong, Gui-Fang Guo, Xiu-Xing Chen, Yan-Qun Xiang, Xuan Li, Hai-Liang Zhang, Yu-Hong Chen, Xue-Lian Xu, Rui-Yan Wu, Yan Yu, Zhi-Ling Li, Xiao-Dan Peng, Yun Huang, Li-Huan Zhou, Gong-Kan Feng, Xiang Guo, Rong Deng, Xiao-Feng Zhu Tags: Research Paper Source Type: research