The Key Laboratory of Geriatrics, Beijing Hospital, National Center of Gerontology, National Health Commission, Institute of Geriatric Medicine, Chinese Academy of Medical Sciences, Beijing, China
Chao Chen
Department of Thoracic Surgery, Peking University Shenzhen Hospital, Shenzhen Peking University, Shenzhen, China; The Hong Kong University of Science and Technology Medical Center, Hong Kong, China
Dong Wei
Department of Urology, Beijing Hospital, National Health Commission, Institute of Geriatric Medicine, Chinese Academy of Medical Sciences, Beijing, China
Yong Xu
Tianjin Institute of Urology, Second Hospital of Tianjin Medical University, Tianjing, China; Department of Urology, Second Hospital of Tianjing Medical University, Tianjing, China
Siying Liang
Genetic Testing Center, Qingdao Women and Children's Hospital, Qingdao, China
Wenlong Jia
Department of Computer Science, City University of Hong Kong, Hong Kong, China
Jian Li
The Key Laboratory of Geriatrics, Beijing Hospital, National Center of Gerontology, National Health Commission, Institute of Geriatric Medicine, Chinese Academy of Medical Sciences, Beijing, China
Yanchun Qu
Tianjin Institute of Urology, Second Hospital of Tianjin Medical University, Tianjing, China
Jianpo Zhai
Department of Urology, Beijing Jishuitan Hospital, Beijing, China
Yaoguang Zhang
Department of Urology, Beijing Hospital, National Health Commission, Institute of Geriatric Medicine, Chinese Academy of Medical Sciences, Beijing, China
Pengjie Wu
Department of Urology, Beijing Hospital, National Health Commission, Institute of Geriatric Medicine, Chinese Academy of Medical Sciences, Beijing, China
Qiang Hao
Department of Urology, Beijing Tian Tan Hospital, Capital Medical University, Beijing, China
Linlin Zhang
School of Nursing, Harbin Medical University, Harbin, China
Wei Zhang
Department of Pathology, Beijing Hospital, National Health Commission, Institute of Geriatric Medicine, Chinese Academy of Medical Sciences, Beijing, China
Xinyu Yang
Department of Urology, Peking University First Hospital, Institute of Urology, Beijing, China
Lin Pan
Clinical Institute of China-Japan Friendship Hospital, Beijing, China
Ruomei Qi
The Key Laboratory of Geriatrics, Beijing Hospital, National Center of Gerontology, National Health Commission, Institute of Geriatric Medicine, Chinese Academy of Medical Sciences, Beijing, China
Yao Li
Department of Surgery, Beijing Hospital, National Health Commission, Institute of Geriatric Medicine, Chinese Academy of Medical Science, Beijing, China
Feiliang Wang
The Department of Ultrasonography, Beijing Hospital, National Health Commission, Institute of Geriatric Medicine, Chinese Academy of Medical Sciences, Beijing, China
Rui Yi
The Key Laboratory of Geriatrics, Beijing Hospital, National Center of Gerontology, National Health Commission, Institute of Geriatric Medicine, Chinese Academy of Medical Sciences, Beijing, China
Ze Yang
The Key Laboratory of Geriatrics, Beijing Hospital, National Center of Gerontology, National Health Commission, Institute of Geriatric Medicine, Chinese Academy of Medical Sciences, Beijing, China
Jianye Wang
Department of Urology, Beijing Hospital, National Health Commission, Institute of Geriatric Medicine, Chinese Academy of Medical Sciences, Beijing, China
The Key Laboratory of Geriatrics, Beijing Hospital, National Center of Gerontology, National Health Commission, Institute of Geriatric Medicine, Chinese Academy of Medical Sciences, Beijing, China
Identification oncogenes is fundamental to revealing the molecular basis of cancer. Here, we found that FOXP2 is overexpressed in human prostate cancer cells and prostate tumors, but its expression is absent in normal prostate epithelial cells and low in benign prostatic hyperplasia. FOXP2 is a FOX transcription factor family member and tightly associated with vocal development. To date, little is known regarding the link of FOXP2 to prostate cancer. We observed that high FOXP2 expression and frequent amplification are significantly associated with high Gleason score. Ectopic expression of FOXP2 induces malignant transformation of mouse NIH3T3 fibroblasts and human prostate epithelial cell RWPE-1. Conversely, FOXP2 knockdown suppresses the proliferation of prostate cancer cells. Transgenic overexpression of FOXP2 in the mouse prostate causes prostatic intraepithelial neoplasia. Overexpression of FOXP2 aberrantly activates oncogenic MET signaling and inhibition of MET signaling effectively reverts the FOXP2-induced oncogenic phenotype. CUT&Tag assay identified FOXP2-binding sites located in MET and its associated gene HGF. Additionally, the novel recurrent FOXP2-CPED1 fusion identified in prostate tumors results in high expression of truncated FOXP2, which exhibit a similar capacity for malignant transformation. Together, our data indicate that FOXP2 is involved in tumorigenicity of prostate.
