TRIM proteins in lung cancer: Mechanisms, biomarkers and therapeutic targets.

The tripartite motif (TRIM) family is defined by the presence of a Really Interesting New Gene (RING) domain, one or two B-box motifs and a coiled-coil region. TRIM proteins play key roles in many biological processes, including innate immunity, tumorigenesis, cell differentiation and ontogenetic development. Alterations in TRIM gene and protein levels frequently emerge in a wide range of tumors and affect tumor progression.

Functional characterization of a potent anti-tumor polysaccharide in a mouse model of gastric cancer.

Aims: Natural polysaccharides are emerging as a new class of immunomodulatory agents due to their potent immunostimulatory effects and suitable biocompatibility. The aim of this study was to identify potent and selective anticancer activity of a bioactive polysaccharide.

Materials And Methods: In vitro, viability assay was performed to screen 16 of bioactive polysaccharides in a panel of normal and cancer cell lines.

Targeting Virus-host Protein Interactions: Feature Extraction and Machine Learning Approaches.

Background: Targeting critical viral-host Protein-Protein Interactions (PPIs) has enormous application prospects for therapeutics. Using experimental methods to evaluate all possible virus-host PPIs is labor-intensive and time-consuming. Recent growth in computational identification of virus-host PPIs provides new opportunities for gaining biological insights, including applications in disease control.

SDADB: a functional annotation database of protein structural domains.

Annotating functional terms with individual domains is essential for understanding the functions of full-length proteins. We describe SDADB, a functional annotation database for structural domains. SDADB provides associations between gene ontology (GO) terms and SCOP domains calculated with an integrated framework.

Probing the functions of long non-coding RNAs by exploiting the topology of global association and interaction network.

Long non-coding RNAs (lncRNAs) are involved in many biological processes, such as immune response, development, differentiation and gene imprinting and are associated with diseases and cancers. But the functions of the vast majority of lncRNAs are still unknown. Predicting the biological functions of lncRNAs is one of the key challenges in the post-genomic era.

Phosphorylation of glutaminase by PKCε is essential for its enzymatic activity and critically contributes to tumorigenesis.

Glutamine metabolism plays an important role in cancer development and progression. Glutaminase C (GAC), the first enzyme in glutaminolysis, has emerged as an important target for cancer therapy and many studies have focused on the mechanism of enhanced GAC expression in cancer cells. However, little is known about the post-translational modification of GAC.

Computational identification of binding energy hot spots in protein-RNA complexes using an ensemble approach.

Motivation: Identifying RNA-binding residues, especially energetically favored hot spots, can provide valuable clues for understanding the mechanisms and functional importance of protein-RNA interactions. Yet, limited availability of experimentally recognized energy hot spots in protein-RNA crystal structures leads to the difficulties in developing empirical identification approaches. Computational prediction of RNA-binding hot spot residues is still in its infant stage.

COMMD9 promotes TFDP1/E2F1 transcriptional activity via interaction with TFDP1 in non-small cell lung cancer.

COMMD protein family is an evolutionarily conserved gene family implicated in a number of critical processes including inflammation, copper homeostasis, sodium balance, endosomal sorting and cancer. In an effort to profile the expression pattern of COMMD family in several non-small cell lung cancer (NSCLC) cell lines, we found that compared with that in human bronchial epithelial (HBE) cells, the mRNA expression levels of five COMMD genes including COMMD3, COMMD4, COMMD5, COMMD6 and COMMD8 were significantly down-regulated, whereas COMMD9 was up-regulated in NSCLC cell lines. Here we reported that the expression of COMMD9 protein was significantly increased in various NSCLC cell lines and tissue samples.

Dihydromyricetin ameliorates oleic acid-induced lipid accumulation in L02 and HepG2 cells by inhibiting lipogenesis and oxidative stress.

Aims: Dihydromyricetin (DMY), a flavonoid component isolated from Ampelopsis grossedentata, was recently reported to ameliorate nonalcoholic fatty liver disease (NAFLD) in patients. However, the underlying mechanisms of this action remain unknown. Here, we evaluate the effect of DMY on an in vitro model of NAFLD and investigate the signal transduction pathways underlying DMY treatment.

Laparoscopic splenectomy and porto-azygos disconnection: clinical research in the treatment of portal hypertension.

To investigate the safety and efficacy of laparoscopic splenectomy and portaazygous devascularization, we studied laparoscopic splenectomy and porto-azygos devascularization patients within the peri-operative period. Clinical data and curative effect are detailed alongside statistical analysis. The laparoscopic splenectomy and porto-azygos devascularization operation time was 2.

TRIM59 Promotes the Proliferation and Migration of Non-Small Cell Lung Cancer Cells by Upregulating Cell Cycle Related Proteins.

TRIM protein family is an evolutionarily conserved gene family implicated in a number of critical processes including inflammation, immunity, antiviral and cancer. In an effort to profile the expression patterns of TRIM superfamily in several non-small cell lung cancer (NSCLC) cell lines, we found that the expression of 10 TRIM genes including TRIM3, TRIM7, TRIM14, TRIM16, TRIM21, TRIM22, TRIM29, TRIM59, TRIM66 and TRIM70 was significantly upregulated in NSCLC cell lines compared with the normal human bronchial epithelial (HBE) cell line, whereas the expression of 7 other TRIM genes including TRIM4, TRIM9, TRIM36, TRIM46, TRIM54, TRIM67 and TRIM76 was significantly down-regulated in NSCLC cell lines compared with that in HBE cells. As TRIM59 has been reported to act as a proto-oncogene that affects both Ras and RB signal pathways in prostate cancer models, we here focused on the role of TRIM59 in the regulation of NSCLC cell proliferation and migration.

Inhibition of mitochondrial glutaminase activity reverses acquired erlotinib resistance in non-small cell lung cancer.

The epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) erlotinib has been approved based on the clinical benefit in non-small cell lung cancer (NSCLC) patients over the past decade. Unfortunately, cancer cells become resistant to this agent via various mechanisms, and this limits the improvement in patient outcomes. Thus, it is urgent to develop novel agents to overcome erlotinib resistance.

Cdc42 induces EGF receptor protein accumulation and promotes EGF receptor nuclear transport and cellular transformation.

Cdc42 is a Ras-related small GTP-binding protein. A previous study has shown that Cdc42 binding to the γ subunit of the coatomer protein complex (γCOP) is essential for Cdc42-regulated cellular transformation, but the molecular mechanism involved is not well understood. Here, we demonstrate that constitutively-active Cdc42 binding to γCOP induced the accumulation of epithelial growth factor receptor (EGFR) in the cells, sustained EGF-stimulated extracellular signal-regulated kinase (ERK), JUN amino-terminal kinase (JNK) and phosphoinositide 3-kinase (PI3K) signaling and promoted cell division.

How does cancer cell metabolism affect tumor migration and invasion?

Cancer metastasis is the major cause of cancer-associated death. Accordingly, identification of the regulatory mechanisms that control whether or not tumor cells become "directed walkers" is a crucial issue of cancer research. The deregulation of cell migration during cancer progression determines the capacity of tumor cells to escape from the primary tumors and invade adjacent tissues to finally form metastases.

Evolutionary method for finding communities in bipartite networks.

An important step in unveiling the relation between network structure and dynamics defined on networks is to detect communities, and numerous methods have been developed separately to identify community structure in different classes of networks, such as unipartite networks, bipartite networks, and directed networks. Here, we show that the finding of communities in such networks can be unified in a general framework-detection of community structure in bipartite networks. Moreover, we propose an evolutionary method for efficiently identifying communities in bipartite networks.