Published in:
01-03-2015 | Research Article
RETRACTED ARTICLE: A comprehensive analysis of candidate genes and pathways in
pancreatic cancer
Authors:
Jie Liu, Jun Li, Hali Li, Aidong Li, Biou Liu, Liou Han
Published in:
Tumor Biology
|
Issue 3/2015
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Abstract
The study aimed to dissect the molecular mechanism of pancreatic cancer
by a range of bioinformatics approaches. Three microarray datasets (GSE32676,
GSE21654, and GSE14245) were downloaded from Gene Expression Omnibus database.
Differentially expressed genes (DEGs) with logarithm of fold change (|logFC|)
>0.585 and p value <0.05 were identified
between pancreatic cancer samples and normal controls. Transcription factors (TFs)
were selected from the DEGs based on TRASFAC database. Gene ontology and Kyoto
Encyclopedia of Genes and Genomes pathway enrichment analyses were performed for the
DEGs using The Database for Annotation, Visualization and Integrated Discovery
(p value <0.05), followed by construction
of protein-protein interaction (PPI) network using Search Tool for the Retrieval of
Interacting Genes software. Latent pathway identification analysis was applied to
analyze the DEGs-related pathways crosstalk and the pathways with high weight value
were included in the pathway crosstalk network using Cytoscape. Sixty-five DEGs were
screened out. CCAAT/enhancer-binding protein delta (CEBPD), FBJ osteosarcoma
oncogene B (FOSB), Stratifin (SFN), Krüppel-like factor 5 (KLF5), Pentraxin 3
(PTX3), and nuclear receptor subfamily 4, group A, member 3 (NR4A3) were important
TFs. Interleukin-6 (IL-6) was the hub node of the PPI network. DEGs were
significantly enriched in NOD-like receptor signaling pathway which was primarily
interacted with inflammation and immune related pathways (cytosolic DNA-sensing,
hematopoietic cell lineage, intestinal immune network for IgA production and
chemokine pathways). The study suggested CEBPD, FOSB, SFN, KLF5, PTX3, NR4A3, IL-6,
and NOD-like receptor pathways were involved in pancreatic cancer.