Hepatoma-Derived Growth Factor and DDX5 Promote Carcinogenesis and Progression of Endometrial Cancer by Activating β-Catenin

Conclusion: Our results provide novel evidence that HDGF interacts with DDX5 and promotes the progression of EC through the induction of β-catenin. Introduction Endometrial cancer (EC) comprises the most common malignancy involving the female genital tract and the fourth most common malignancy in women after breast, lung, and colorectal cancers (1). In 2012, approximately 320,000 new cases of EC were diagnosed worldwide and the incidence is increasing (2). Currently, endometrial carcinogenesis is thought to be a multi-step process involving the coordinated interaction of hormonal regulation, gene mutation, adhesion molecules, and apoptosis; however, the molecular mechanisms underlying the pathogenesis of EC have not been fully elucidated (3). Therefore, a better understanding of the molecular mechanism underlying the progression of EC will likely lead to new insights regarding novel therapeutic targets. Hepatoma-derived growth factor (HDGF), the gene for which is located on chromosome 1q21–23, is a heparin-binding growth factor that was originally purified from media conditioned with the human hepatoma cell line, HuH7 (4). HDGF is ubiquitously expressed in normal tissues and tumor cell lines that exhibit growth factor properties. The most recent study reported that HDGF acts as a coactivator of SREBP1-mediated transcription of lipogenic genes (5). HDGF is characterized as a mitogen for many cell types and localizes to the nucleus, which is necessary for...
Source: Frontiers in Oncology - Category: Cancer & Oncology Source Type: research