Androgen regulated ECD overexpression promotes prostate cancer tumorigenesis through increased glycolysis

Prostate cancer (PC) is the second most common cancer in men worldwide. Androgen receptor (AR)-mediated signaling is essential for PC tumorigenesis and use of AR inhibitors is the first line of therapy until patients develop androgen-resistant PC. Here, we report that the mammalian orthologue of the drosophila ecdysoneless (ECD) mRNA and protein are overexpressed in PC patient tissues as compared to hyperplastic prostate tissues, and its overexpression predicts shorter survival in patients. RNA-seq analysis of mouse tumors revealed increase mRNA levels of several glycolytic genes in ECD-overexpressing tumors. Our results support a novel role of androgen regulated ECD overexpression in PC tumorigenesis through direct ECD binding and stabilization of mRNAs of key glycolytic genes. Overall design: Total RNA-seq of modified human LNCaP xenografted tumors after 37 days. LNCaP cells were modified to overexpress ECD and compared with control LNCaP tumors.