HoxA10 Induces Proliferation in Human Prostate Carcinoma PC-3 Cell Line

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• 作者：Baoxiu Li (1)
  Xiaofei Cao (1)
  Chengyin Weng (1)
  Yong Wu (1)
  Xisheng Fang (1)
  Xiaoshi Zhang (2)
  Guolong Liu (1)
  
• 关键词：HoxA10 ; Prostate cancer ; Lentivirus ; Cancer cell line ; Cell proliferation
• 刊名：Cell Biochemistry and Biophysics
• 出版年：2014
• 出版时间：November 2014
• 年：2014
• 卷：70
• 期：2
• 页码：1363-1368
• 全文大小：905 KB
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• 作者单位：Baoxiu Li (1)
  Xiaofei Cao (1)
  Chengyin Weng (1)
  Yong Wu (1)
  Xisheng Fang (1)
  Xiaoshi Zhang (2)
  Guolong Liu (1)
  
  1. Department of Oncology, Guangzhou First People鈥檚 Hospital, Guangzhou Medical University, Guangzhou, 510180, China
  2. State Key Laboratory of Oncology in South China, Cancer Center, Sun Yat-Sen University, Guangzhou, 510060, China
  
• ISSN：1559-0283

文摘

The objectives of this study were to examine the expression levels of Homeobox A10 (HoxA10) in prostate cancer cells and to study the molecular mechanism of HoxA10-mediated regulation of prostate cancer cell growth and development. We investigated the effect of HoxA10 on cell proliferation by stably overexpressing or silencing HoxA10 in prostate cancer PC-3 cell line using lentiviral vectors. Quantitative real-time PCR and western blotting analysis were used to compare the expressions of HoxA10 in prostate cancer cell lines and normal prostate epithelium. Cancer cell proliferation was examined by MTT assay and colony formation assay. The levels of HoxA10 expression were significantly increased in prostate cancer cell lines and tissues compared to those in normal prostate epithelium. Overexpression of HoxA10 in PC-3 cells induced significant cancer cell proliferation, whereas silencing of HoxA10 expression by RNAi resulted in decreased proliferation rates. HoxA10 was highly expressed in prostate cancer cells and tissues, suggesting its functional involvement in cancer cell proliferation. We successfully overexpressed or silenced HoxA10 in prostate cancer PC-3 cell line and discovered that the levels of HoxA10 directly correlate with cancer cell proliferation. These findings contribute to a better understanding of the regulatory mechanism of HoxA10 in prostate cancer.