p90/CIP2A mediates breast cancer cell proliferation and apoptosis

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• 作者：Xinxin Liu (1) (2)
  Bo Peng (1)
  Yang Li (1)
  Ningjing Lei (1)
  Wenjie Li (2)
  Jian-Ying Zhang (1)
  
• 关键词：Breast cancer ; p90/CIP2A ; Cell proliferation ; Apoptosis ; shRNA knockdown
• 刊名：Molecular Biology Reports
• 出版年：2014
• 出版时间：November 2014
• 年：2014
• 卷：41
• 期：11
• 页码：7471-7478
• 全文大小：1,549 KB
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• 作者单位：Xinxin Liu (1) (2)
  Bo Peng (1)
  Yang Li (1)
  Ningjing Lei (1)
  Wenjie Li (2)
  Jian-Ying Zhang (1)
  
  1. Department of Biology Sciences, The University of Texas at El Paso, El Paso, TX, 79968, USA
  2. College of Public Health, Zhengzhou University, Zhengzhou, 450001, Henan, China
  
• ISSN：1573-4978

文摘

Cancerous inhibitor of PP2A (p90/CIP2A) was recently characterized as an innovative oncoprotein in human malignancies. p90/CIP2A inhibited c-Myc-associated PP2A phosphatase activity to promote cell proliferation and tumor growth. A growing number of studies have demonstrated that the overexpression of p90/CIP2A in various human malignancies. But the function of p90/CIP2A in cancer progression is still poorly understood. In the current research, we aim to explore the biological function of p90/CIP2A in breast cancer. shRNA knockdown was performed in MDA-MB-231 and LM2-4 cell lines. Cell proliferation assay, colony formation assay and flow cytometry were carried out to evaluate the role of p90/CIP2A in cell proliferation and apoptosis. p90/CIP2A depletion in breast cancer cells inhibited proliferation and increased paclitaxel-induced apoptosis. Furthermore, p90/CIP2A silencing down-regulated the expression of c-Myc and the level of p-ERK1/2. Taken together, our data suggest that p90/CIP2A as a crucial oncoprotein has been involved in cell proliferation and apoptosis, which may serve as a therapeutic target in breast cancer treatment.