Abstract
We aimed to identify STK31 as a cancer-testis (CT) gene and to explore its potential clinical value, regulatory mechanisms, and gene network in pancreatic cancer (PC). Gene expression data were generated from normal organ samples and pancreatic cancer samples from three public databases. STK31 expression patterns in normal and PC tissues were identified, and we explored its regulatory mechanisms. Gene ontology (GO) and pathway analyses of STK31-related genes were performed and an STK31 protein–protein interaction (PPI) network was constructed. STK31 was confirmed as a CT gene in PC and its expression was significantly higher in patients with new neoplasm compared with patients without new neoplasm (P = 0.046) and in more advanced pathologic stages than in earlier stages (P = 0.002); methylation level correlated negatively with STK31 expression. In total, 757 STK31-related genes were identified, and were significantly enriched in terms of polymorphisms and alternative splicings. The PPI network predicted that STK31 was physically associated with the PIWI (originally P-element Induced WImpy testis in Drosophila) and Tudor families.
Highlights
pancreatic cancer (PC) is a highly malignant digestive tract disease with difficult early diagnosis and treatment
To determine whether STK31 could be assigned to the CT genes expressed in PC, we first evaluated its expression pattern in normal human tissues including pancreas using transcriptomic data deposited in the Genotype-Tissue Expression Project (GTEx)
The Human Protein Atlas (HPA) result was generally consistent with the GTEx data, showing that STK31 was only expressed in the testis at both RNA and protein level (Figure 1B & 1D)
Summary
PC is a highly malignant digestive tract disease with difficult early diagnosis and treatment. Previous studies have suggested four major driver genes of PC: KRAS (Kras proto-oncogene, GTPase), CDKN2A (cyclindependent kinase inhibitor 2A), TP53 (tumor protein p53), and SMAD4 (SMAD family member 4). Patient-derived xenograft models of pancreatic ductal adenocarcinoma (PDAC) showed that JQ1, an inhibitor of CT genes in the bromodomain and extraterminal (BET) protein family (BRDT), suppresses PDAC development by inhibiting both MYC (v-myc avian myelocytomatosis viral oncogene homolog) activity and inflammatory signals www.impactjournals.com/oncotarget [11]. This provided new insight into the molecular targets of PC.
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