Dysregulated expression of homeobox family genes may influence survival outcomes of patients with epithelial ovarian cancer: analysis of data from The Cancer Genome Atlas

// Kyung Jin Eoh 1 , Hee Jung Kim 1 , Jung-Yun Lee 1 , Eun Ji Nam 1 , Sunghoon Kim 1 , Sang Wun Kim 1 and Young Tae Kim 1 1 Institute of Women’s Medical Life Science, Department of Obstetrics and Gynecology, Yonsei University College of Medicine, Seoul, Korea Correspondence to: Young Tae Kim, email: ytkchoi@yuhs.ac Keywords: carcinogenesis, epithelial ovarian cancer, homeobox genes, survival, TCGA Received: June 11, 2017      Accepted: June 30, 2017      Published: August 01, 2017 ABSTRACT Homeobox (HOX) family genes encode key transcription factors for embryogenesis and may be correlated with carcinogenesis. The aim of this study was to elucidate whether aberrant expression of HOX genes influences outcomes in epithelial ovarian cancer (EOC). Gene expression data and clinicopathologic information from 630 patients with EOC were downloaded from The Cancer Genome Atlas database. We explored correlations between expression levels of HOX gene family members and clinicopathological variables. Higher expression of HOXA1 , A4 , A5 , A7 , A10 , A11 , B13 , C13 , D1 , and D3 was associated with advanced FIGO stage. Suboptimal residual disease after debulking surgery was significantly correlated with higher expression of HOXB9 , B13 , and C13 . Additionally, patients with high expression of HOXC6 and C11 were significantly more likely to have poor performance status. Overall survival was significantly shorter in patients with high, rather than low, expression of two HOX genes ( HOXA10 and B3 ), and significantly longer in patients with high rather than low HOXC5 expression. Dysregulated expression of the HOXA10 , B3 , and C5 was significantly correlated with overall survival in EOC patients. HOX gene expression levels are potentially useful as a prognostic indicator in EOC, and HOX genes may represent a novel and promising target for anticancer therapeutics.