DEK Is a Potential Biomarker Associated with Malignant Phenotype in Gastric Cancer Tissues and Plasma.

Gastric cancer (GC) is the second most widespread cause of cancer-related mortality worldwide. The discovery of novel biomarkers of oncoproteins can facilitate the development of therapeutic strategies for GC treatment. In this study, we identified novel biomarkers by integrating isobaric tags for relative and absolute quantitation (iTRAQ), a human plasma proteome database, and public Oncomine datasets to search for aberrantly expressed oncogene-associated proteins in GC tissues and plasma. One of the most significantly upregulated biomarkers, DEK, was selected and its expression validated. Our immunohistochemistry (IHC) (n = 92) and quantitative real-time polymerase chain reaction (qRT-PCR) (n = 72) analyses disclosed a marked increase in DEK expression in tumor tissue, compared with paired nontumor mucosa. Importantly, significantly higher preoperative plasma DEK levels were detected in GC patients than in healthy controls via enzyme-linked immunosorbent assay (ELISA). In clinicopathological analysis, higher expression of DEK in both tissue and plasma was significantly associated with advanced stage and poorer survival outcomes of GC patients. Data from receiver operating characteristic (ROC) curve analysis disclosed a better diagnostic accuracy of plasma DEK than carcinoembryonic antigen (CEA), carbohydrate antigen 19.9 (CA 19.9), and C-reactive protein (CRP), highlighting its potential as an effective plasma biomarker for GC. Plasma DEK is also more sensitive in tumor detection than the other three biomarkers. Knockdown of DEK resulted in inhibition of GC cell migration via a mechanism involving modulation of matrix metalloproteinase MMP-2/MMP-9 level and vice versa. Our results collectively support plasma DEK as a useful biomarker for making diagnosis and prognosis of GC patients.

Contribution of genetic polymorphisms of stromal cell-derived factor-1 and its receptor, CXCR4, to the susceptibility and clinicopathologic development of oral cancer.

BACKGROUND: The aim of this study was to evaluate the relations of SDF-1 and its receptor, CXCR4, gene variants on oral cancer risk. METHODS: PCR-RFLP was used to measure SDF-1-3'A and CXCR4 gene polymorphisms in 284 controls and 113 patients with oral cancer. RESULTS: After being adjusted for age, individuals with A/G heterozygotes of SDF-1 had a higher risk of 1.86-fold to develop oral cancer when compared with those with G/G wild type homozygotes. Furthermore, patients with oral cancer with at least 1 mutant T allele of CXCR4 gene had a risk of 2.66-fold to progress to stage III or IV. CONCLUSIONS: SDF-1-3'A gene polymorphism may be considered as a factor of increased susceptibility to oral cancer, and at least 1 mutated T allele of CXCR4 gene is associated with the development of stage III or IV and the induction of lymph-node metastasis of oral cancer disease in Taiwanese.