The short isoform of PRLR suppresses the pentose phosphate pathway and nucleotide synthesis through the NEK9-Hippo axis in pancreatic cancer
Hui Nie, Pei-Qi Huang, Shu-Heng Jiang, Qin Yang, Li-Peng Hu, Xiaomei Yang, Jun Li, Yahui Wang, Qing Li, Yifan Zhang, Lei Zhu, Yanli Zhang, Yanqiu Yu, Gary Guishan Xiao, Yongwei Sun, Jianguang Ji, Zhigang Zhang
Abstract
Our characterization of the relationship between PRLR-SF signaling, the NEK9-Hippo pathway, PPP and nucleotide synthesis explains a mechanism for the correlation between PRLR-SF and metabolic reprogramming in PDAC progression. Strategies to alter this pathway might be developed for the treatment or prevention of pancreatic cancer.
Topics & Concepts
BiologyCancer researchPancreatic cancerGene isoformProlactin receptorPentose phosphate pathwayCancerGlycolysisEndocrinologyProlactinBiochemistryGeneMetabolismHormoneGeneticsHippo pathway signaling and YAP/TAZCancer-related Molecular PathwaysMicrotubule and mitosis dynamics