2-Zinc-glycoprotein 1 (AZGP1) is a multidisciplinary protein that participates in many important functions in the human body, including fertilization, immunoregulation and lipid mobilization. Recently, it has been shown that AZGP1 is also involved in carcinogenesis and tumor differentiation. In this study, we investigated the expression levels and prognostic value of AZGP1 in primary gastric cancers. We examined the expression of AZGP1 in 35 paired cancerous and matched adjacent noncancerous gastric mucosa tissues by real-time quantitative RT-PCR (qRT-PCR) and western blotting. Furthermore, we analyzed AZGP1 expression in 248 patients who underwent resection procedures between 2005 and 2007 using immunohistochemistry. The relationships between the AZGP1 expression levels, the clinicopathological factors, and patient survival were investigated. AZGP1 expression was significantly reduced at both the mRNA (P = 0.023) and protein levels (P = 0.019) in tumor tissue samples, compared with expression in matched adjacent non-tumor tissue samples. The immunohistochemical staining data showed that AZGP1 expression was significantly decreased in 52.8% (131/248) of gastric adenocarcinoma cases. Clinicopathological analysis showed that the reduced expression of AZGP1 was significantly correlated with tumor location (P = 0.011), histological grade (P = 0.005) and T stage (P = 0.008). Kaplan–Meier survival curves revealed that the reduced expression of AZGP1 was associated with a poor prognosis in gastric adenocarcinoma patients (P = 0.009). Multivariate Cox analysis identified AZGP1 expression was an independent prognostic factor for overall survival of gastric adenocarcinoma patients (HR = 1.681, 95% CI = 1.134–2.494, P = 0.011). Our study suggests that AZGP1 might serve as a candidate tumor suppressor and a potential prognostic biomarker in gastric carcinogenesis.

The haptens 4-[[(2,3-dihydro-2,2-dimethyl-7-benzofuranyloxy)carbonyl]-amino]butanoic acid (BFNB) and 6-[((2,3-dihydro-2,2-dimethyl-7-benzofuranyloxy)-carbonylamino]hexanoic acid (BFNH) were synthesized and then used to develop a rapid,specific and sensitive ELISA method to determine residues of the pesticide carbofuran in avariety of matrices. A hybridoma cell line (5D3) producing anti-carbofuran monoclonalantibodies (MAbs) was also established. Based on the MAbs in combination with theheterologous hapten BFNH coupled to either horseradish peroxidase (HRP) or ovalbumin(OVA), four ELISAs (formats I-IV) for the quantification of carbofuran were developedand compared. Among them, the optimized format II (the conjugate-coated directcompetitive ELISA) showed the best characteristics, with an IC50 value of 18.49 ng/mL, alimit of detection of 0.11 ng/mL and the shortest assay time (1 h). This ELISA method wasthen applied to the determinations of carbofuran in environmental water, soil and foodsamples. The relative standard deviations (R.S.D.s) ranged from 1.8% to 21.3% and themean recoveries were 104.6%, 108.3%, 106.3% and 100.1% for water, soil, lettuce andcabbage, respectively. Thus, the ELISA method of format II exhibited the potential todevelop commercial ELISA kits for a rapid detection of carbofuran for human health andenvironmental safety.

// <![CDATA[ $('.header-date').hide();$('#titleAuthors').hide();$('#abstractHeader').hide(); // ]]> Chang-Long Chen1,2,*, Ying Wang1,3,*, Qiu-Zhong Pan1,2, Yan Tang1,2, Qi-Jing Wang2, Ke Pan1,2, Li-Xi Huang2, Jia He2, Jing-Jing Zhao1,2, Shan-Shan Jiang1,2, Xiao-Fei Zhang1,2, Hong-Xia Zhang1,2, Zi-Qi Zhou1,2, De-Sheng Weng1,2 and Jian-Chuan Xia1,2 1 Collaborative Innovation Center for Cancer Medicine, State Key Laboratory of Oncology in South China, Sun Yat-Sen University Cancer Center, Guangzhou, China 2 Department of Biotherapy, Sun Yat-Sen University Cancer Center, Guangzhou, China 3 Department of Epidemiology and Health Statistics, Guangdong Key Laboratory of Molecular Epidemiology, Guangdong Pharmaceutical University, Guangzhou, China * These authors have contributed equally to this work Correspondence to: Jian-Chuan Xia, email: // <![CDATA[ mail("xiajch","mail.sysu.edu",23,"") // ]]> De-Sheng Weng, email: // <![CDATA[ mail("wengdsh","sysucc.org",23,"") // ]]> Keywords: BRD7, tumor suppressor, hepatocellular carcinoma, prognosis, tumorigenicity Received: December 15, 2015 Accepted: February 08, 2016 Published: February 23, 2016

Ubiquitination factor E4B (UBE4B) has been speculated to have contradictory functions upon tumorigenesis as an oncogene or tumor suppressor in different types of cancers. We investigated the expression and prognostic role of UBE4B in primary hepatocellular carcinoma (HCC) using cell lines and 149 archived HCC samples. Correlation between the functions of UBE4B in HCC was also explored. We used human HCC cell lines (HepG2, Hep3B, SK‐Hep1, Huh7, SMMC‐7721, BEL‐7402) and a normal hepatocyte cell line (LO2) along with HCC samples from patients who had undergone resection for HCC previously at our hospital. A battery of methods (real‐time quantitative polymerase chain reaction; Western blotting; immunohistochjemical analyses; cell proliferation and colony formation assays; cell migration and cell invasion assays) were employed to assess various aspects of UBE4B.We found that UBE4B expression was upregulated aberrantly at mRNA and protein levels in human primary HCC tissues. Amplified expression of UBE4B was highly correlated with poor outcome. Silencing of UBE4B expression by siRNA inhibited the proliferation, colony formation, migration and invasion of HCC cells in vitro, and resulted in significant apoptosis that was associated with downregulation of expression of Bcl‐2 and upregulation of expression of total p53, p‐p53, Bax and Cleaved‐Caspase3 in HCC cells. Our findings suggested that UBE4B might have an oncogenic role in human primary HCC, and that it could be used as a prognostic marker (as well as a potential molecular target) for the treatment of HCC.

Background: High frequency of loss of heterozygosity (LOH) was found at D7S486 in primary gastric cancer (GC). And we found a high frequency of LOH region on 7q31 in primary GC from China, and identified D7S486 to be the most frequent LOH locus. This study was aimed to determine what genes were affected by the LOH and served as tumor suppressor genes (TSGs) in this region. Here, a high-throughput single nucleotide polymorphisms (SNPs) microarray fabricated in-house was used to analyze the LOH status around D7S486 on 7q31 in 75 patients with primary GC. Western blot, immunohistochemistry, and RT-PCR were used to assess the protein and mRNA expression of TESTIN (TES) in 50 and 140 primary GC samples, respectively. MTS assay was used to investigate the effect of TES overexpression on the proliferation of GC cell lines. Mutation and methylation analysis were performed to explore possible mechanisms of TES inactivation in GC.Results: LOH analysis discovered five candidate genes (ST7,FOXP2,MDFIC,TESandCAV1) whose frequencies of LOH were higher than 30%. However, onlyTESshowed the potential to be a TSG associated with GC. Among 140 pairs of GC samples, decreasedTESmRNA level was found in 96 (68.6%) tumor tissues when compared with matched non-tumor tissues (p< 0.001). Also, reduced TES protein level was detected in 36 (72.0%) of all 50 tumor tissues by Western blot (p= 0.001). In addition, immunohistochemical staining result was in agreement with that of RT-PCR and Western blot. Down regulation of TES was shown to be correlated with tumor differentiation (p= 0.035) and prognosis (p= 0.035, log-rank test). Its overexpression inhibited the growth of three GC cell lines. Hypermethylation ofTESpromoter was a frequent event in primary GC and GC cell lines. However, no specific gene mutation was observed in the coding region of theTESgene.Conclusions: Collectively, all results support the role ofTESas a TSG in gastric carcinogenesis and thatTESis inactivated primarily by LOH and CpG island methylation.

A steric-hindrance regulated probe NBD-2FDCI for self-adaptive detection of biothiols and H ₂ S in human urine and living cells.