Up-regulated lnc-SNHG1 contributes to osteosarcoma progression through sequestration of miR-577 and activation of WNT2B/Wnt/ß-catenin pathway.

Long noncoding RNA small nucleolar RNA host gene 1 (lnc-SNHG1) was reported to play an oncogenic role in the progression of cancers. However, the roles of SNHG1 and its molecular mechanism in osteosarcoma (OS) cells are largely unknown. In present study, we found that the expression of SNHG1 was up-regulated in OS tissues and cell lines. OS patients with the high SNHG1 expression were positively correlated with tumor size, TNM stage and lymph node metastasis. In addition, SNHG1 overexpression promoted cell proliferation, cell migration and EMT process in U2OS and MG63 cells and tumor growth in vivo. Furthermore, we also found that miR-577 could act as a ceRNAof SNHG1 in OS cells and the promotion of OS progression induced by lnc-SNHG1 overexpression required the inactivity of miR-577. Besides, we identified that WNT2B acted as a target of miR-577, and WNT2B played the oncogenic role in OS cells by activating Wnt/ß-catenin pathway. In short, our study suggested that lnc-SNHG1 could promote OS progression via miR-577 and WNT2B. The lnc-SNHG1/miR-577/WNT2B/Wnt/ß-catenin axis regulatory network might provide a potential new therapeutic strategy for OS treatment.

MicroRNA-208b inhibits human osteosarcoma progression by targeting ROR2.

MicroRNAs are widely involved in cancer progression by inhibiting the expression levels of oncogenes or tumor suppressor genes, and dysregulation of microRNAs may contribute to tumorigenesis. Here, we found that overexpressed miR-208b can reduce the proliferation of human osteosarcoma cell lines U-2OS and Saos-2 by arresting cell cycle progression. The in vivo xenograft tumors induced by Saos-2 cells overexpressing miR-208b had smaller size and grew more slowly than those induced by the control cells. The mobility of U-2OS or Saos-2 cells was also downregulated by miR-208b. MiR-208b targeted a site in the 3' untranslated region of receptor tyrosine kinase-like orphan receptor 2. Inhibition of receptor tyrosine kinase-like orphan receptor 2 suppresses osteosarcoma metastasis in vitro. Recovering the expression levels of receptor tyrosine kinase-like orphan receptor 2 in miR-208b-overexpressed U-2OS or Saos-2 cells attenuated the inhibitory effects of miR-208b. In addition, the expression levels of miR-208b are significantly reduced in human osteosarcoma tissue samples compared to normal tissue samples, and miR-208b levels correlated inversely with receptor tyrosine kinase-like orphan receptor 2 levels. On these bases, we identified that miR-208b targets receptor tyrosine kinase-like orphan receptor 2 gene by which miR-208b can regulate the development of osteosarcoma.

Two functional polymorphisms in microRNAs and lung cancer risk: a meta-analysis.

MicroRNAs are involved in several biological processes including cell apoptosis and proliferation, stress resistance, and fat metabolism, and act as tumor suppressors by malignant transformation of human cells. The aim of this study was to identify the associations of single nucleotide polymorphisms (SNPs) rs11614913 and rs3746444 with lung cancer risk. In this meta-analysis with 2,219 cases and 2,232 controls for SNP rs11614913 and 1,685 cases and 1,690 controls for SNP rs3746444, we summarized five case-control studies by searching databases of PubMed, EMBASE, and Chinese National Knowledge Infrastructure (CNKI). Lung cancer risk associated with the two SNPs was estimated by odd ratios (ORs) with 95% confidence intervals (CIs). SNP rs11614913 (OR 0.88, 95% CI 0.78-1.00 for TT vs. CT + CC) was found to be potentially associated with a decreased risk of lung cancer. However, we found no association between SNP rs3746444 and lung cancer risk. In the subgroup analysis by ethnicity, a negative association was also observed in Asians for SNP rs11614913, but a nonsignificant association for SNP rs3746444. Our meta-analysis provides evidence for potential protective effects on lung cancer risk associated with SNP rs11614913, particularly in Asian populations. Further, larger studies are necessary to validate the findings.

Connexin43 and AMPK Have Essential Role in Resistance to Oxidative Stress Induced Necrosis.

Reactive oxygen species (ROS) induced oxidative stress leads to cell damage and neurological disorders in astrocytes. The gap junction protein connexin43 (Cx43) could form intercellular channels in astrocytes and the expression of Cx43 plays an important role in protecting the cells from damage. In the present study, we investigated the contribution of Cx43 to astrocytic necrosis induced by the ROS hydrogen peroxide (H2O2) and the mechanism by which AMPK was involved in this process. Fluorescence microscopy, flow cytometry, and western blot were used quantitatively and qualitatively to determine the cell apoptosis, necrosis, and protein expression. Lack of Cx43 expression or blockage of Cx43 channels resulted in increased H2O2-induced astrocytic necrosis, supporting a cell protective effect of functional Cx43 channels. Our data suggest that AMPK is important for Cx43-mediated ROS resistance. Inhibition of AMPK activation results in reduction of necrosis and ROS production. Taken together, our findings suggest that the role of Cx43 in response to H2O2 stress is dependent on the activation of AMPK signaling pathways and regulates ROS production and cell necrosis.

Association between epidermal growth factor receptor mutations and the expression of excision repair cross-complementing protein 1 and ribonucleotide reductase subunit M1 mRNA in patients with non-small cell lung cancer.

The present study aimed to investigate the association between epidermal growth factor receptor (EGFR) gene mutations and excision repair cross-complementing protein 1 (ERCC1) and ribonucleotide reductase subunit M1 (RRM1) mRNA expression in non-small cell lung cancer (NSCLC) tissue. The quantitative polymerase chain reaction was used to detect EGFR mutations, and ERCC1 and RRM1 mRNA expression in 257 cases of NSCLC. In the NSCLC samples the EGFR mutation rate was 49.03% (126/257). The rate was higher in females and non-smoking patients (P<0.05). High expression of ERCC1 mRNA was observed in 47.47% of the samples (122/257), while a high RRM1 mRNA expression was observed in 61.87% of the samples (159/257). In comparison with patients with NSCLC without EGFR mutations, patients with EGFR mutations had significantly lower levels of ERCC1 mRNA expression (P<0.05); however, EGFR mutations and expression levels of RRM1 mRNA were not correlated in NSCLC tissues (P>0.05). In addition, ERCC1 mRNA expression was not correlated with the expression levels of RRM1 mRNA (P>0.05). In conclusion, patients with NSCLC with EGFR mutations tend to have a low expression of ERCC1 mRNA and may potentially benefit from platinum-based chemotherapy.

Comparison of prevalence of metabolic syndrome between korean emigrants and host country residents in Japan and china-the korean emigrant study.

OBJECTIVES: This study aims to compare the prevalence of metabolic syndrome between Korean emigrants (KEs) and their host country residents in Japan and China. METHODS: The Korean Emigrant Study (KES) is a cohort study initiated in 2005 to elucidate the effect of genetic susceptibility and environmental change on hypertension, diabetes, and metabolic syndrome. Equal numbers of KEs and host country residents, aged 30 or over, were recruited from three regions; Kobe-Osaka in Japan (total number=965), Yanbian in China (n=1,019), and Changchun in China (n=949). RESULTS: The age-adjusted prevalences of metabolic syndrome among KEs in Kobe-Osaka were significantly higher than those among Japanese (in men 24.0% vs. 15.6%, p=0.04, in women 8.4% vs. 2.7%, p=0.01), while the age-adjusted prevalences among KEs in Changchun were similar to those among Chinese (in men 11.7% vs. 16.1%, p=0.37, in women 28.3% vs. 30.1%, p=0.91). The age-adjusted prevalences were generally higher in Yanbian than other regions, and KEs had higher prevalence than Chinese in men but not in women (in men 37.9% vs. 28.3%, p=0.03, women 46.0% vs. 50.6%, p=0.44). The components with significant ethnic differences in prevalence were high blood pressure and abdominal obesity in Japan, and triglyceride in China. The most influential component in diagnosing metabolic syndrome was abdominal obesity in men and triglyceride in women. CONCLUSION: The prevalence of metabolic syndrome was higher in KEs than in host country residents in Japan but not in China. Abdominal obesity and triglyceride are both discriminating and influential components in metabolic syndrome.

Epidemiology of hepatitis E in Northeastern China, South Korea and Japan.

OBJECTIVES: The seroprevalence of hepatitis E virus (HEV) infection in Northeastern Asia is unknown. This study was conducted to gain insight into the epidemiology of HEV that has been obscure in Northeastern China, South Korea and Japan. METHODS: A total of 1500 samples of serum were collected (300 each) from 5 groups of inhabitants over 40 years of age (Korean Chinese, indigenous Chinese, South Koreans, Koreans living in Japan, and indigenous Japanese) and screened for antibodies to HEV by the antigen-antibody-antigen sandwich Enzyme Linked Immunosorbent Assay system. RESULTS: The positivity for HEV antibodies was 50.7% (95%CI: 45.0-56.3) in Korean Chinese, 47.7% (95%CI: 42.1-53.3) in indigenous Chinese, 34% (95%CI: 28.9-39.5) in South Koreans, 14.3% (95%CI: 10.8-18.8) in Koreans living in Japan, and 6.0% (95%CI: 3.8-9.3) in indigenous Japanese. CONCLUSIONS: This result emphasizes that HEV is endemic in Northeastern Asia and tends to accumulate in developing countries. Further studies are needed to elucidate the genotype of HEV circulating in these areas and its transmission route-water-borne outbreaks, smaller outbreaks or sporadic forms attributed to zoonosis-with reference to past epidemics, food culture, and sanitary conditions.