Khon Kaen, Thailand
Khon Kaen, Thailand

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Suwanrungruang K.,Cancer Unit | Wiangnon S.,Khon Kaen University
Asian Pacific Journal of Cancer Prevention | Year: 2015

Background: Colorectal cancer (CRC) is one of the most common cancers worldwide. This study aimed to investigate the risk factors for colorectal cancer in the Thai population. Materials and Methods: A cohort study was carried out in Khon Kaen, Thailand, including 71 cases of histologically confirmed CRC patients among 19,861 participants, aged 30-69 years, who were recruited for a cohort study during the period 1990-2001. Participants were followed-up until 31 December, 2013. To identify factors associated with the incidence of colorectal cancer, hazard ratios were evaluated using Cox proportional hazard regression. Results: No environmental variables could be shown to be significantly related to the risk of CRC. Although in our sample, CRC was more prevalent among males, ex-smokers, and those who drank alcohol beverages = 50 gram/day, but we could not demonstrate significantly associations (HRmale ≥ 1.67, 95% CI, 0.80-3.49, HR ex-smokers = 1.34, 95% CI, 0.52-3.46, and HRalc ≥ 50 = 1.08, 95% CI, 0.43-2.71). Individuals within the sample with a family history of cancer, working hour > 8 hours per day, and current-smokers appeared to have decrease risk of CRC, but again these relationship could not be shown to be significantly associated (HRfam cancer= 0.96, 95% CI, 0.85-1.09, HRwork > 8= 0.84, 95% CI, 0.36-1.93, and HRcurrent-smoker = 0.51, 95% CI, 0.18-1.38). Conclusions: We found no evidence of environmental factors effecting the risk of CRC. There is a need for further research to determine why factors identified risk in other populations appear to not be associated with CRC risk in Thais.


Rodriguez M.S.,Cancer Unit | Egana I.,CIC BioGUNE | Lopitz-Otsoa F.,CIC BioGUNE | Aillet F.,Cancer Unit | And 7 more authors.
Cell Death and Disease | Year: 2014

Accurate regulation of nuclear factor-κB (NF-κB) activity is crucial to prevent a variety of disorders including immune and inflammatory diseases. Active NF-κB promotes IκBα and A20 expression, important negative regulatory molecules that control the NF-κB response. In this study, using two-hybrid screening we identify the RING-type zinc-finger protein 114 (RNF114) as an A20-interacting factor. RNF114 interacts with A20 in T cells and modulates A20 ubiquitylation. RNF114 acts as negative regulator of NF-κB-dependent transcription, not only by stabilizing the A20 protein but also IκBα. Importantly, we demonstrate that in T cells, the effect of RNF114 is linked to the modulation of T-cell activation and apoptosis but is independent of cell cycle regulation. Altogether, our data indicate that RNF114 is a new partner of A2O involved in the regulation of NF-κB activity that contributes to the control of signaling pathways modulating T cell-mediated immune response. © 2014 Macmillan Publishers Limited All rights reserved.


PubMed | Hematological Diseases, Cancer Unit, Cytometry and Advanced Optical Microscopy Core Facility and CIC bioGUNE
Type: | Journal: Cell death & disease | Year: 2014

Accurate regulation of nuclear factor-B (NF-B) activity is crucial to prevent a variety of disorders including immune and inflammatory diseases. Active NF-B promotes IB and A20 expression, important negative regulatory molecules that control the NF-B response. In this study, using two-hybrid screening we identify the RING-type zinc-finger protein 114 (RNF114) as an A20-interacting factor. RNF114 interacts with A20 in T cells and modulates A20 ubiquitylation. RNF114 acts as negative regulator of NF-B-dependent transcription, not only by stabilizing the A20 protein but also IB. Importantly, we demonstrate that in T cells, the effect of RNF114 is linked to the modulation of T-cell activation and apoptosis but is independent of cell cycle regulation. Altogether, our data indicate that RNF114 is a new partner of A2O involved in the regulation of NF-B activity that contributes to the control of signaling pathways modulating T cell-mediated immune response.


El Zein N.,Pediatric Oncology Laboratory | D'Hondt S.,Pediatric Oncology Laboratory | Sariban E.,Pediatric Oncology Laboratory | Sariban E.,Cancer Unit
Cellular Signalling | Year: 2010

The G-protein coupled receptor (GPCR) fMLP receptor (FPR) and the two receptors tyrosine kinase (RTK), the nerve growth factor (NGF) receptor TrkA and the epidermal growth factor (EGF) receptor (EGFR) are involved in reactive oxygen species (ROS), matrix metalloproteinase-9 (MMP-9) production and CD11b membrane integrin upregulation. We show that in monocytes the three receptors crosstalk each other to modulate these pro-inflammatory mediators. Tyrphostin AG1478, the EGFR inhibitor, inhibits fMLP and NGF-associated ROS production, fMLP-associated CD11b upregulation and NGF-induced TrkA phosphorylation; K252a, the NGF receptor inhibitor, inhibits fMLP or EGF-associated ROS production, CD11b expression and EGF-induced EGFR phosphorylation; cyclosporine H, the FPR inhibitor inhibits EGF or NGF-associated ROS production, EGF-associated CD11b upregulation and prevents EGFR and TrkA phosphorylation by their respective ligand EGF and NGF. In response to fMLP, TrkA phosphorylation is inhibited by the EGFR inhibitor while EGFR phosphorylation is inhibited by the TrkA inhibitor. Receptor crosstalks are Src and ERK dependent. Down-regulation of each receptor by specific siRNA suppresses the ability of the two other receptors to promote ligand-mediated ERK phosphorylation and pro-inflammatory activities including ROS, MMP-9 production and CD11b upregulation. Thus, in monocytes GPCR ligands' activity involves activation of RTK while RTK-ligands activity engages GPCR-signalling molecules. © 2010 Elsevier Inc.


Urena E.,University Pompeu Fabra | Pirone L.,CIC bioGUNE | Chafino S.,University Pompeu Fabra | Perez C.,CIC bioGUNE | And 8 more authors.
Molecular Biology and Evolution | Year: 2016

SUMOylation, the covalent binding of Small Ubiquitin-like Modifier (SUMO) to target proteins, is a posttranslational modification that regulates critical cellular processes in eukaryotes. In insects, SUMOylation has been studied in holometabolous species, particularly in the dipteran Drosophila melanogaster, which contains a single SUMO gene (smt3). This has led to the assumption that insects contain a single SUMO gene. However, the analysis of insect genomes shows that basal insects contain two SUMO genes, orthologous to vertebrate SUMO1 and SUMO2/3. Our phylogenetical analysis reveals that the SUMO gene has been duplicated giving rise to SUMO1 and SUMO2/3 families early in Metazoan evolution, and that later in insect evolution the SUMO1 gene has been lost after the Hymenoptera divergence. To explore the consequences of this loss, we have examined the characteristics and different biological functions of the two SUMO genes (SUMO1 and SUMO3) in the hemimetabolous cockroach Blattella germanica and compared them with those of Drosophila Smt3. Here, we show that the metamorphic role of the SUMO genes is evolutionary conserved in insects, although there has been a regulatory switch from SUMO1 in basal insects to SUMO3 in more derived ones. We also show that, unlike vertebrates, insect SUMO3 proteins cannot form polySUMO chains due to the loss of critical lysine residues within the N-terminal part of the protein. Furthermore, the formation of polySUMO chains by expression of ectopic human SUMO3 has a deleterious effect in Drosophila. These findings contribute to the understanding of the functional consequences of the evolution of SUMO genes. © The Author 2015. Published by Oxford University Press on behalf of the Society for Molecular Biology and Evolution.


PubMed | University Pompeu Fabra, Cancer Unit, Ikerbasque and CIC bioGUNE
Type: Journal Article | Journal: Molecular biology and evolution | Year: 2016

SUMOylation, the covalent binding of Small Ubiquitin-like Modifier (SUMO) to target proteins, is a posttranslational modification that regulates critical cellular processes in eukaryotes. In insects, SUMOylation has been studied in holometabolous species, particularly in the dipteran Drosophila melanogaster, which contains a single SUMO gene (smt3). This has led to the assumption that insects contain a single SUMO gene. However, the analysis of insect genomes shows that basal insects contain two SUMO genes, orthologous to vertebrate SUMO1 and SUMO2/3. Our phylogenetical analysis reveals that the SUMO gene has been duplicated giving rise to SUMO1 and SUMO2/3 families early in Metazoan evolution, and that later in insect evolution the SUMO1 gene has been lost after the Hymenoptera divergence. To explore the consequences of this loss, we have examined the characteristics and different biological functions of the two SUMO genes (SUMO1 and SUMO3) in the hemimetabolous cockroach Blattella germanica and compared them with those of Drosophila Smt3. Here, we show that the metamorphic role of the SUMO genes is evolutionary conserved in insects, although there has been a regulatory switch from SUMO1 in basal insects to SUMO3 in more derived ones. We also show that, unlike vertebrates, insect SUMO3 proteins cannot form polySUMO chains due to the loss of critical lysine residues within the N-terminal part of the protein. Furthermore, the formation of polySUMO chains by expression of ectopic human SUMO3 has a deleterious effect in Drosophila. These findings contribute to the understanding of the functional consequences of the evolution of SUMO genes.

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