Abstract:Objective: To clarify the association of IL-6 polymorphisms and periodontitis, a meta-analysis of case-control studies and a systemic review were conducted. Material and methods: We performed a literature search using PubMed and Medline database to May 2009, with no restrictions. We also reviewed references from all retrieved articles. Six case-control studies involving 1 093 periodontitis cases and 574 controls were selected for meta-analysis to assess the purported associations between IL-6 polymorphisms and the risk of periodontitis. IL-6 −174 G/C and −572 C/G polymorphisms were included in the present meta-analysis, and the association between IL-6 −6331 T/C polymorphism and the risk of periodontitis was adequately reviewed as well. Results and conclusion: The present meta-analysis indicates that the IL-6 −174 G allele could not modify the risk of chronic periodontitis, but increased the risk of aggressive periodontitis. And −572 C/G polymorphism is associated with the pathogenesis of periodontitis, including chronic periodontitis or aggressive periodontitis.

Long non-coding RNA nuclear-enriched abundant transcript 1 (NEAT1) plays an important role in the pathogenesis and development of several types of cancer. However, the functional mechanism of NEAT1 in hepatocellular carcinoma (HCC) remains unclear. NEAT1 and microRNA (miR)-129-5p expression in HCC tissues and cell lines was quantified by means of quantitative PCR. The effects of NEAT1 expression inhibition or upregulation in HCC cell lines were analyzed in terms of cell viability and apoptosis. Biological software was used to predict the binding sites of NEAT1 and miR-129-5p. The expression of the miR-129-5p target molecules valosin-containing protein (VCP) and IκB was detected using Western blotting. The effect of NEAT1 on tumor growth was observed in mouse models of transplanted hepatoma. In the present study, it was concluded that the expression of NEAT1 was significantly increased in the HCC tissues and cell lines. Meanwhile, after downregulating NEAT1 expression in HepG2/Huh7 cell lines, the cell viability was significantly lowered, whereas the corresponding rate of apoptosis was significantly increased. Additionally, it was found that the NEAT1 and miR-129-5p expression showed a negative correlation in HCC tissues. It was further proved that there was a certain negative regulatory mechanism between NEAT1 and miR-129-5p, which was related to the expression of VCP and IκB. The mouse model experiments confirmed that the interference with NEAT1 expression inhibited tumor growth. The study concluded that the overexpression of NEAT1 inhibited the expression of miR-129-5p by regulating VCP/IκB, thereby promoting the proliferation of HCC cells. This study provides new insights into the pathogenesis of HCC, as well as identifying new target genes for diagnosis and treatment. The results provide strong evidence that upregulated NEAT1 promotes the proliferation of cancer cells in hepatocellular carcinoma (HCC) and this regulatory mechanism depends on the microRNA (miR)-129-5p-valosin-containing protein-IκB axis. The study also indicates that NEAT1 could be a potential therapeutic target for HCC.

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BackgroundExperimental data suggest that mitochondria is involved in tumorigenesis. However, little is known about the qualitative and quantitative changes of mtDNA in colorectal cancer tissues. We therefore conducted possible correlations of the mitochondrial DNA (mtDNA) copy number in colorectal cancer (CRC) with clinical and pathological findings and CRC prognosis.MethodsmtDNA copy numbers in CRC cancer tissue and adjacent non-cancerous tissue samples were measured using quantitative real-time polymerase chain reaction analyses from 60 patients admitted to our hospital. We examined the correlation of mtDNA copy numbers and clinicopathologic parameters of CRC patients. The correlation between mtDNA copy number and three-year survival was analyzed.ResultsThe mtDNA copy number was lower in CRC tissue compared with the corresponding non-cancerous colorectal tissue (mean: 108.60 ± 20.11 vs. 153.68 ± 25.72) and was significantly correlated with lymph-node metastasis. Patients with a lower mtDNA copy number tended to have lower 3-year survival than patients with a higher mtDNA copy number assessed by Kaplan–Meier curves, but the correlation was not significant (overall survival, 63.0 vs 83%).ConclusionsThese results suggest that a reduced copy number of mtDNA is correlated with malignant potential in CRC.

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The aim of this study was to investigate the role of NEAT1 in hepatocellular carcinoma (HCC), and probe whether NEAT1 participate in the epithelial-mesenchymal transition (EMT) and metastasis regulated by HIF-2α. Expression of lncRNA NEAT1 was initially assessed in HCC tissues and in a series of HCC cell lines. The correlations between NEAT1 levels and HIF-2α were analyzed through plasmid vector construction. The potential underlying mechanisms of NEAT1 in HCC were performed through in vitro and in vivo functional assays. Expression of NEAT1, HIF-2α were significantly increased in HCC tissues and cell lines. Then, in vitro assays revealed that NEAT1 promotes EMT and metastasis by stimulating the inactivation of HIF-2α in HCC. An in vivo animal model also demonstrated the cancer promotion mechanism of NEAT1. In this study, we found that the NEAT1 was high expression in HCC. NEAT1 promotes tumor cell EMT, migration and invasion capacities by stimulating the activation of HIF-2α in HCC.

The operational agility literature suffers from a lack of clarity in terms of the process or underlying mechanisms through which operational agility is achieved. Drawing on the information processing view of the firm, this study attempts to address this gap by examining the process of operational agility development. A process model of developing information processing capability for operational agility is proposed. As the model suggests, operational agility is achieved through a twostep process -the construction of IT-enabled information processing network and the implementation of organizational control -to enhance the right information processing capability. We further identify three types of information processing capability -information sensitivity, information synergy and information fluiditythat enable operational agility. Furthermore, a five-step practical guide for developing information processing capability for operational agility is provided for practitioners. This is achieved by conducting a case study of Haier, one of the largest household appliance manufacturers in China. This paper concludes with a discussion of the potential contributions and directions for future research.

Jasmonates (JAs) regulate various stress responses and development processes in plants, and the JA pathway is tightly controlled. In this study, we report the functional characterization of two novel RING-type ubiquitin ligases, RING DOMAIN LIGASE3 (RGLG3) and RGLG4, in modulating JA signaling. Both RGLG3 and RGLG4 possessed ubiquitin ligase activities and were widely distributed in Arabidopsis (Arabidopsis thaliana) tissues. Altered expression of RGLG3 and RGLG4 affected methyl JA-inhibited root growth and JA-inductive gene expression, which could be suppressed by the coronatine insensitive1 (coi1) mutant. rglg3 rglg4 also attenuated the inhibitory effect of JA-isoleucine-mimicking coronatine on root elongation, and consistently, rglg3 rglg4 was resistant to the coronatine-secreting pathogen Pseudomonas syringae pv tomato DC3000, suggesting that RGLG3 and RGLG4 acted in response to the coronatine and promoted JA-mediated pathogen susceptibility. In addition, rglg3 rglg4 repressed wound-stunted plant growth, wound-stimulated expression of JA-responsive genes, and wound-induced JA biosynthesis, indicating their roles in JA-dependent wound response. Furthermore, both RGLG3 and RGLG4 responded to methyl JA, P. syringae pv tomato DC3000, and wounding in a COI1-dependent manner. Taken together, these results indicate that the ubiquitin ligases RGLG3 and RGLG4 are essential upstream modulators of JA signaling in response to various stimuli.