Gene expression profiling of the synergy of 5-aza-2′-deoxycytidine and paclitaxel against renal cell carcinomaReportar como inadecuado




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World Journal of Surgical Oncology

, 10:183

First Online: 06 September 2012Received: 04 April 2012Accepted: 08 August 2012

Abstract

BackgroundRenal cell carcinoma RCC is one of the most common kidney cancers and is highly resistant to chemotherapy. We previously demonstrated that 5-aza-2-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.

MethodscDNA 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.

ResultsWe 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.

ConclusionThe 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.

KeywordsSynergy 5-aza-2-deoxycytidine Paclitaxel Renal cell carcinoma PI3K-Akt Electronic supplementary materialThe online version of this article doi:10.1186-1477-7819-10-183 contains supplementary material, which is available to authorized users.

Tiandong Han, Donghao Shang contributed equally to this work.

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Autor: Tiandong Han - Donghao Shang - Xiuhong Xu - Ye Tian

Fuente: https://link.springer.com/



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