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Gene Expression Profile of Hedgehog Signaling Pathway Inhibition in Human Carcinoma Cells
TANG Xiaoli 1,DENG Libin 2,ZHANG Weilong 2,GAO Meng 3,HUANG Dengliang 3,LUO Shiwen 3,LU Quqin 4 *
1.School of Medicine, Nanchang University, Nanchang, Jiangxi, 330001, China
2.Institute of Translational Medicine, Nanchang University, Nanchang, Jiangxi,330001, China
3.Center for Experimental Medicine, the First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, 330006, China
4.School of Public Health, Nanchang University, Nanchang, Jiangxi 330006, China
*Correspondence author
#Submitted by
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Funding: none
Opened online:17 March 2014
Accepted by: none
Citation: TANG Xiaoli,DENG Libin,ZHANG Weilong.Gene Expression Profile of Hedgehog Signaling Pathway Inhibition in Human Carcinoma Cells[OL]. [17 March 2014] http://en.paper.edu.cn/en_releasepaper/content/4589220
 
 
Background: Aberrant activation of the Hedgehog (Hh) signaling pathway frequency occurs in human cancers, and increased evidence implicates the considerable role of GANT61 (Gli-ANTagonist, a kind of Hh signaling inhibitor) in anticancer therapy. However, it is still lacking the systematic scanning for the common mechanism of various cancer cells in respond to Hh-inhibition. Methodology/Principal Findings: Gene expression profiling of Hh inhibited HT-29 and MKN45 cells was determined by Illumina? Sentrix? BeadChip arrays. From the 17,329 expressed genes across genome, we identified 668 and 269 differentially expressed genes (DEGs, p < 0.01) in comparison pairs of HT-29 and MKN45, respectively. Interesting, large number of common DEGs (77 genes) were seen in both two comparison pairs, which was clearly more than the predicted number (10, p < 10?4). Further interpretation of gene ontology was based on over-representation analysis. Two nested categories of GO biological processes ("cell death", and "response to stimulus") were detected as candidates with the enrichments of DEGs in both two cell lines. In addition, cDNA microarray profiling of extra cancer cells (ES2 and H4) verified the change of expression in six common DEGs related to "cell death" (CDKN1A, DDIT3, IER3, IL8, MFGE8, and PPP1R15A) following GANT61 treatment. Conclusions/Significance: Our research indicates that inhibition of Hh has considerable effect on genes from pathway of "cell death" in various carcinoma cells. And, the aberrant of "response to DNA damage" related genes (such as DDIT3) may play a critical role in GANT61-induced cell death. In summary, this dataset provide insight into the molecular mechanisms of GANT61-induced antitumor activity, and the list of novel GLI-targets in cancer cells.
Keywords:Hedgehog signaling pathways; GANT61; Differentially Expressed Gene; anticancer therapy
 
 
 

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