Gene expression profiling of the synergy of 5-aza-2-/sup>-deoxycytidine and paclitaxel against renal cell carcinoma

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• 作者：Tiandong Han (1)
  Donghao Shang (1)
  Xiuhong Xu (1)
  Ye Tian (1)
  
• 关键词：Synergy ; 5 ; aza ; 2-deoxycytidine ; Paclitaxel ; Renal cell carcinoma ; PI3K/Akt
• 刊名：World Journal of Surgical Oncology
• 出版年：2012
• 出版时间：December 2012
• 年：2012
• 卷：10
• 期：1
• 全文大小：790KB
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• 作者单位：Tiandong Han (1)
  Donghao Shang (1)
  Xiuhong Xu (1)
  Ye Tian (1)
  
  1. Department of Urology, Beijing Friendship Hospital, Capital Medical University, 95 Yong-An Road, Beijing, 100050, China
  

文摘

Background Renal cell carcinoma (RCC) is one of the most common kidney cancers and is highly resistant to chemotherapy. We previously demonstrated that 5-aza-2-/sup>-deoxycytidine (DAC) could significantly increase the susceptibility of renal cell carcinoma (RCC) cells to paclitaxel (PTX) treatment in vitro, and showed the synergy of DAC and PTX against RCC. The purpose of this study is to investigated the gene transcriptional alteration and investigate possible molecular mechanism and pathways implicated in the synergy of DAC and PTX against RCC. Methods cDNA microarray was performed and coupled with real-time PCR to identify critical genes in the synergistic mechanism of both agents against RCC cells. Various patterns of gene expression were observed by cluster analysis. IPA software was used to analyze possible biological pathways and to explore the inter-relationships between interesting network genes. Results We found that lymphoid enhancer-binding factor 1 (LEF1), transforming growth factor β-induced (TGFBI), C-X-C motif ligand 5 (CXCL5) and myelocytomatosis viral related oncogene (c-myc) may play a pivotal role in the synergy of DAC and PTX. The PI3K/Akt pathway and other pathways associated with cyclins, DNA replication and cell cycle/mitotic regulation were also associated with the synergy of DAC and PTX against RCC. Conclusion The activation of PI3K/Akt-LEF1/β-catenin pathway could be suppressed synergistically by two agents and that PI3K/Akt-LEF1/β-catenin pathway is participated in the synergy of two agents.