The prostate cancer-up-regulated myc-associated zinc-finger protein (MAZ) modulates proliferation and metastasis through reciprocal regulation of androgen receptor

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• 作者：Li Jiao (1) (2)
  Yun Li (1) (3)
  Dan Shen (1) (4)
  Chuanliang Xu (1)
  Linhui Wang (1)
  Gang Huang (1)
  Lin Chen (2)
  Yinhui Yang (1)
  Chun Yang (1)
  Yongwei Yu (5)
  Yinghao Sun (1)
  
• 关键词：Myc ; associated zinc ; finger protein ; Androgen receptor ; Prostate cancer ; siRNA
• 刊名：Medical Oncology
• 出版年：2013
• 出版时间：June 2013
• 年：2013
• 卷：30
• 期：2
• 全文大小：721KB
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• 作者单位：Li Jiao (1) (2)
  Yun Li (1) (3)
  Dan Shen (1) (4)
  Chuanliang Xu (1)
  Linhui Wang (1)
  Gang Huang (1)
  Lin Chen (2)
  Yinhui Yang (1)
  Chun Yang (1)
  Yongwei Yu (5)
  Yinghao Sun (1)
  
  1. Department of Urology, Changhai Hospital, Second Military Medical University, 168 Changhai Road, Shanghai, 200433, P. R. China
  2. Tongji University Advanced Institute of Translational Medicine, Shanghai, P.R. China
  3. Department of Urology, Shanghai Shibei Hospital of Zhabei District, Shanghai, 200443, China
  4. Department of Urology, Chinese People’s Liberation Army General Hospital, Beijing, China
  5. Department of Pathology, Changhai Hospital, Second Military Medical University, Shanghai, P.R. China
  

文摘

Prostate cancer (PCa) is one of the most commonly diagnosed malignancies in men and the second leading cause of male cancer mortality. MAZ (Myc-associated zinc-finger protein) is a transcription factor that regulates the transcription of oncogenes, and the deregulated MAZ expression is closely related to the development and progression of a variety of cancers. In the present study, the role of MAZ in PCa tumorigenesis and its interaction with androgen receptor (AR), which is essential to PCa development in humans, were investigated. MAZ expression was found to be higher in clinical PCa specimens than in benign prostatic hyperplasia (BPH) and adjacent normal tissues, and MAZ expression was positively correlated with AR expression, which was also observed in PCa cell lines. After knockdown of MAZ by siRNA, cell proliferation was notably inhibited, colony formation declined, the cell cycle was arrested at G0/G1 phase, and the number of cells in S phase decreased (p?<?0.05). MAZ knockdown resulted in a significant decline in the migration and invasion capacity of the LNCaP-AD cell line. siRNA knockdown of AR significantly decreased MAZ expression, and knockdown of MAZ significantly increased the expression of AR and DHT-induced androgen response element (ARE). These results suggest that MAZ and AR are interrelated and that MAZ plays an important role in PCa pathogenesis, which could be a potential therapeutic target.