BackgroundSyndecan-1 plays a vital role in the suppression, transformation, and migration of several cancer types, including colorectal cancer (CRC). However, the prognostic and clinical significance of syndecan-1 in CRC remains conflicting. Therefore, we performed a meta-analysis to clarify this relationship.MethodsA comprehensive literature search for relevant studies published up to December 2014 was performed using PubMed, EMBASE, and Ovid library database. The odds ratio (OR) and pooled hazard ratio (HR) with their 95 % confidence intervals (CI) were used to estimate the effects.ResultsTen studies with 888 CRC patients were selected for evaluation. The results showed that syndecan-1 expression was lower in CRC tissue than in normal colorectal tissue (OR = 0.02, 95 % CI = 0.00–0.09), and lower in the advanced stage than in the early stage (OR = 2.24, 95 % CI = 1.14 − 4.42). Additionally, syndecan-1 expression was higher in well and moderately differentiated CRC than in poorly differentiated CRC (OR = 2.91, 95 % CI = 1.21–6.98); no significant difference was found in patients with or without lymph node metastasis (OR = 0.91, 95 % CI = 0.34–2.43) and distant metastasis (OR = 0.89, 95 % CI = 0.19-4.21). The pooled results showed that syndecan-1 expression was not associated with survival in CRC patients (HR = 0.93, 95 % CI = 0.86–1.01).ConclusionThis meta-analysis indicated that loss of syndecan-1 expression is associated with CRC development, histological differentiation, and clinical stage, but not with lymph node metastasis and distant metastasis. In addition, these findings fail to support the prognostic significance of syndecan-1 in CRC.

ObjectiveThe mechanism underlying colon cancer metastasis remain unclear. This study aimed to elucidate the genes alteration during the metastasis of colon cancer and identify genes that crucial to the metastasis and survival of colon cancer patients.MethodsThe dataset of primary and metastasis tissue of colon cancer, and dataset of high and low metastasis capability of colon cancer cells were selected as training cohort, and the overlapped differentially expressed genes (DEGs) were screened from the training cohort. The functional enrichment analysis for the overlapped DEGs was performed. The prognostic value of overlapped DEGs were analyzed in The Cancer Genome Atlas dataset, and a gene signature was developed using genes that related to the overall survival (OS). The prognostic value of the gene signature was further confirmed in a validation cohort.ResultsA total of 184 overlapped DEGs were screened from the training cohort. Functional enrichment analysis revealed the significant gene functions and pathways of the overlapped DEGs. Four hub genes (3-oxoacid CoA-transferase 1, actinin alpha 4, interleukin 8, integrin subunit alpha 3) were identified using protein–protein network analysis. Six genes (aldehyde dehydrogenase 2, neural precursor cell expressed, developmentally down-regulated 9, filamin A, lamin B receptor, twinfilin actin binding protein 1, serine and arginine rich splicing factor 1) were closely related to the OS of colon cancer patients. A gene signature was developed using these six genes based on their risk score, and the validation cohort indicated that the prognostic value of this gene signature was high in the prediction of colon cancer patients.ConclusionsOur study demonstrates a gene profiles related to the metastasis of colon cancer, and identify a six-gene signature that acts as an independent biomarker on the prognosis of colon cancer.

The aim of the present study was to identify potential prognostic microRNA (miRNA) biomarkers for colon adenocarcinoma (COAD) prognostic prediction using the dataset of The Cancer Genome Atlas (TCGA). The genome-wide miRNA sequencing dataset and corresponding COAD clinical information were downloaded from TCGA. Prognosis-related miRNA screening was performed by genome-wide multivariable Cox regression analysis and used for prognostic signature construction. Ten miRNAs (hsa-mir-891a, hsa-mir-6854, hsa-mir-216a, hsa-mir-378d-1, hsa-mir-92a-1, hsa-mir-4709, hsa-mir-92a-2, hsa-mir-210, hsa-mir-940 and hsa-mir-887) were identified as prognostic miRNAs and used for further prognostic signature construction. The 10-miRNA prognostic signature showed good performance in prognosis prediction (adjusted P<0.0001; adjusted hazard ratio, 4.580; 95% confidence interval, 2.783–7.538). In the time-dependent receiver operating characteristic analysis, the area under the curve was 0.735, 0.788, 0.806, 0.806, 0.775 and 0.900 for 1-, 2-, 3-, 4-, 5- and 10-year COAD overall survival prediction, respectively. Comprehensive survival analysis suggested that the 10-miRNA prognostic signature is an independent prognostic factor in COAD, with a better performance in COAD overall survival prediction than other traditional clinical parameters. Functional enrichment indicated that the corresponding target genes were significantly enriched in multiple biological processes and pathways, including regulation of cell proliferation, cell cycle, cell growth, and Wnt and transforming growth factor-β signaling pathways. In conclusion, our present study identified a 10-miRNA expression signature that may serve as a potential prognostic biomarker in COAD patients.

Previous studies have reported that alcohol dehydrogenase (ADH) isoenzymes possess diagnostic value in gastric cancer (GC). However, the prognostic value of ADH isoenzymes in GC remains unclear. The aim of the present study was to identify the prognostic value of ADH genes in patients with GC. The prognostic value of ADH genes was investigated in patients with GC using the Kaplan-Meier plotter tool. Kaplan-Meier plots were used to assess the difference between groups of patients with GC with different prognoses. Hazard ratios (HR) and 95% confidence intervals (CI) were used to assess the relative risk of GC survival. Overall, 593 patients with GC and 7 ADH genes were included in the survival analysis. High expression of ADH 1A (class 1), α polypeptide (ADH1A; log-rank P=0.043; HR=0.79; 95% CI: 0.64–0.99), ADH 1B (class 1), β polypeptide (ADH1B; log-rank P=1.9×10−05; HR=0.65; 95% CI: 0.53–0.79) and ADH 5 (class III), χ polypeptide (ADH5; log-rank P=0.0011; HR=0.73; 95% CI: 0.6–0.88) resulted in a significantly decreased risk of mortality in all patients with GC compared with patients with low expression of those genes. Furthermore, protective effects may additionally be observed in patients with intestinal-type GC with high expression of ADH1B (log-rank P=0.031; HR=0.64; 95% CI: 0.43–0.96) and patients with diffuse-type GC with high expression of ADH1A (log-rank P=0.014; HR=0.51; 95% CI: 0.3–0.88), ADH1B (log-rank P=0.04; HR=0.53; 95% CI: 0.29–0.98), ADH 4 (class II), π polypeptide (log-rank P=0.033; HR=0.58; 95% CI: 0.35–0.96) and ADH 6 (class V) (log-rank P=0.037; HR=0.59; 95% CI: 0.35–0.97) resulting in a significantly decreased risk of mortality compared with patients with low expression of those genes. In contrast, patients with diffuse-type GC with high expression of ADH5 (log-rank P=0.044; HR=1.66; 95% CI: 1.01–2.74) were significantly correlated with a poor prognosis. The results of the present study suggest that ADH1A and ADH1B may be potential prognostic biomarkers of GC, whereas the prognostic value of other ADH genes requires further investigation.