Pancreatic ductal adenocarcinoma (PDAC) is a leading cause of cancer death worldwide. Our study aimedto reveal molecular mechanisms. Microarray data of GSE15471 (including 39 matching pairs of pancreatictumor tissues and patient-matched normal tissues) was downloaded from Gene Expression Omnibus (GEO)database. We identified differentially expressed genes (DEGs) in PDAC tissues compared with normal tissues bylimma package in R language. Then GO and KEGG pathway enrichment analyses were conducted with onlineDAVID. In addition, principal component analysis was performed and a protein-protein interaction networkwas constructed to study relationships between the DEGs through database STRING. A total of 532 DEGs wereidentified in the 38 PDAC tissues compared with 33 normal tissues. The results of principal component analysisof the top 20 DEGs could differentiate the PDAC tissues from normal tissues directly. In the PPI network, 8 ofthe 20 DEGs were all key genes of the collagen family. Additionally, FN1 (fibronectin 1) was also a hub nodein the network. The genes of the collagen family as well as FN1 were significantly enriched in complement andcoagulation cascades, ECM-receptor interaction and focal adhesion pathways. Our results suggest that genes ofcollagen family and FN1 may play an important role in PDAC progression. Meanwhile, these DEGs and enrichedpathways, such as complement and coagulation cascades, ECM-receptor interaction and focal adhesion may beimportant molecular mechanisms involved in the development and progression of PDAC.