Abstract. Hepatitis B virus (HBV) infection has been shown by certain studies to be associated with diabetes mellitus (DM); however, the results of these studies were controversial. For that reason, a meta-analysis of the literature was performed in order to determine the association between HBV infection and the prevalence of DM more accurately. The PubMed, Embase, Chinese National Knowledge Infrastructure and Wan Fang databases, as well as the Chinese Science and Technology Journal Database, were searched for literature published until June 2014. The reference lists of all relevant articles were also searched. The summary odds ratios (ORs) and their corresponding 95% confidence intervals (95% CIs) were calculated based on a random-effects model. Heterogeneity was assessed using the I 2 statistic. Subgroup analyses were conducted based on study type and region for the purpose of assessing the factors that could potentially affect the outcome. A total of 15 eligible studies (in 14 articles) were selected for the meta-analysis, involving 12,974,690 HBV-infected patients and 231,776,232 controls. The OR for the prevalence of DM was 1.33 (95% CI, 1.09-1.62; P=0.005) between the patients with HBV infection and the controls. The subgroup analysis based on study type revealed a significantly higher prevalence of DM in the HBV-infected group than that in the control group in both case-control (OR, 1.89; 95% CI, 1.08-3.30; P=0.025) and cross-sectional (OR, 1.41; 95% CI, 1.04-1.90; P=0.027) studies. The subgroup analysis based on region revealed a significantly higher prevalence of DM in the HBV-infected group than in the control group in the Asia-Pacific region (OR, 1.67; 95% CI, 1.08-2.58; P=0.022). Compared with uninfected patients, the pooled results suggest that HBV-infected patients have a higher risk of developing DM; however, given the fact that this is a meta-analysis of observational studies, further randomized controlled trials are required in order to reach a more accurate conclusion.

Epithelial-mesenchymal transition (EMT) is a vital process in epithelial cancer invasion and metastasis. The induction of EMT by Six1 has been described as a common mode of cancer progression, which could promote breast cancer migration and invasion. In the study, we found that miR-204-5p could suppress the migration and invasion of breast cancer cell lines. Since overexpression of Six1 promote EMT, we identified a mechanism by which miR-204-5p inhibited the EMT by downregulating the Six1, which was mediated by a conserved miR-204-5p seed-matching sequence in the 3'-UTR of Six1 mRNA. We also identified that upregulation of Six1 could downregulate miR-204-5p expression, affecting the migration and invasion of breast cancer cell lines. In conclusion, the frequent upregulation of Six1 and/or downregulation of miR-204-5p in breast cancer may shift the equilibrium of these reciprocal regulations and lock breast cancer cells in the mesenchymal state.

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Abstract. Sushi domain containing 2 (SUSD2) has been identified as a gene encoding an 822-amino acid protein, which contains a transmembrane domain and functional domains inherent to adhesion molecules. Previous studies have reported that increased expression of SUSD2 has a critical role in tumorigenesis in human breast cancer. However, to the best of our knowledge, SUSD2 expression status and its correlation with the clinicopathological features of non-small cell lung cancer (NSCLC) have not previously been investigated. In the present study, reverse transcription-quantitative polymerase chain reaction and western blotting were used to evaluate SUSD2 messenger RNA (mRNA) and protein expression in NSCLC and adjacent normal lung tissues. The clinicopathological significance of SUSD2 was investigated by immunohistochemical analysis of an NSCLC tissue microarray. Receiver operating characteristic analysis was used to determine the cut-off score for positive expression of SUSD2. Furthermore, the correlation between SUSD2 expression and the clinicopathological features of NSCLC was analyzed by χ 2 test. The results revealed that SUSD2 mRNA (P<0.0001) and protein (P<0.0001) expression levels were significantly decreased in NSCLC tissues compared with those of adjacent normal tissues. When the SUSD2 positive expression percentage was determined to be >47.5% (area under ROC curve, 0.799; P<0.000), positive expression of SUSD2 was observed in 100% (32/32) of normal lung tissues and 55% (88/160) of NSCLC tissues by immunohistochemistry (χ 2 =21.160; P<0.000). Furthermore, it was demonstrated that the reduced SUSD2 protein levels in cancer tissues were positively correlated with poor histological grade (χ 2 =41.764; P<0.000), advanced clinical stage (χ 2 =10.790; P=0.013), higher pT (χ 2 =9.070; P=0.028) and positive regional lymph node metastasis (χ 2 =15.399; P=0.002).In conclusion, these data suggest that the reduced expression of SUSD2 is associated with the progression of NSCLC and may have a role in the pathogenesis of NSCLC.