-
DNA and cell biology 05/2012; 31(5):648-50. · 2.28 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: To investigate the relationship between the promoter polymorphism of IL6 (-174G > C, -572G > C and -597G > A) and chronic rhinosinusitis (CRS).
The case-control study consisted of 123 patients with CRS and 239 controls from a Chinese Han population from Shanghai. The genotypes of the subjects were determined by polymerase chain reaction-restriction fragment length polymorphism and gene sequencing. Besides, the concentrations of the totle immunoglobulin E (TIgE) and eosinophilic cationic protein (ECP) in the blood were also determined.
The -174G > C and -597G > A polymorphisms were not detected in this study population. Significant differences in genotype and allele frequencies of -572C/G were observed between CRS patients and control groups. In CRS patients, the CC, CG, GG genotype frequencies were 69.1%, 29.3%, 1.6%, C, G allele frequencies were 83.7%, 16.3%. In control group, the genotype frequencies were 55.2%, 42.3%, 2.5%, the allele frequencies were 76.4%, 23.6%, respectively. The -572CC genotype was associated with an increased risk of developing CRS (P < 0.05, OR = 1.932, 95% CI, 1.205-3.097). There was no significant differences in the concentrations of the TIgE and ECP among each genotype.
IL-6 gene -572G > C polymorphism is associated with the susceptibility to CRS. CC genotype could be an independent risk factor.
Lin chuang er bi yan hou ke za zhi = Journal of clinical otorhinolaryngology 03/2012; 26(5):197-200, 204.
-
[show abstract]
[hide abstract]
ABSTRACT: We aimed to explore the role of allele A/G single nucleotide polymorphism (SNP) of gene Interleukin 10 (IL-10) promoter-1082 in the susceptibility to gastric cancer through a systematic review and meta-analysis. Each initially included article was scored for quality appraisal. Desirable data were extracted and registered into databases. Twenty studies were ultimately eligible for the meta-analysis of IL-10-1082 A/G SNP. We adopted the most probably appropriate genetic model (dominant model), with the combined group of GG-plus-GA genotypes compared with the AA genotype. Potential sources of heterogeneity were sought out via subgroup analyses and sensitivity analyses, and publication biases were estimated. Between IL-10-1082 GG-plus-GA genotypes with the risk of developing gastric cancer, statistically significant association could be noted with overall gastric cancer, being mainly in Asian subgroup, large sample subgroup, high quality subgroup, intestinal-type subgroup, cardia-type subgroup, and some genotyping method subgroups. Our meta-analysis indicates that IL-10-1082 GG-plus-GA genotypes are associated with the overall risk of developing gastric cancer and seem to be more susceptible to overall gastric cancer in Asian populations. IL-10-1082 GG-plus-GA genotypes are more associated with the pathologically intestinal-type gastric cancer or anatomically cardia-type gastric cancer.
DNA and cell biology 02/2012; 31(4):582-91. · 2.28 Impact Factor
-
DNA and cell biology 02/2012; · 2.28 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: DRAM is a lysosomal membrane protein and is critical for p53-mediated autophagy and apoptosis. DRAM has a potential tumor-suppressive function and is downregulated in many human cancers. However, the regulation of DRAM expression is poorly described so far. Here, we demonstrated that serum deprivation strongly induces DRAM expression in liver cancer cells and a core DNA sequence in the DRAM promoter is essential for its responsiveness to serum deprivation. We further observed that euchromatin markers for active transcriptions represented by diacetyl-H3, tetra-acetyl-H4 and the trimethyl-H3K4 at the core promoter region of DRAM gene are apparently increased in a time-dependent manner upon serum deprivation, and concomitantly the dimethyl-H3K9, a herterochromatin marker associated with silenced genes, was time-dependently decreased. Moreover, the chromatin remodeling factor Brg-1 is enriched at the core promoter region of the DRAM gene and is required for serum deprivation induced DRAM expression. These observations lay the ground for further investigation of the DRAM gene expression.
PLoS ONE 01/2012; 7(12):e50502. · 4.09 Impact Factor
-
DNA and cell biology 12/2011; · 2.28 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: A high performance liquid chromatography method with ultraviolet and fluorimetric detection has been developed for the simultaneous determination of urinary creatinine (Cr), tryptophan (Trp) and three Trp-related metabolites including kynurenine (Kyn), kynurenic acid (Kyna) and 5-hydroxyindole-3-acetic acid (5-HIAA). Samples were pretreated by centrifugation after a freeze-thaw cycle to remove protein and other precipitates. Separation was achieved by an Agilent HC-C18 (2) analytical column and a gradient elution program with a constant flow rate 1mL/min at an ambient temperature. Total run time was 30 min. Cr, Kyn and Kyna were measured by a variable wavelength detector at wavelengths 258 nm, 365 nm and 344 nm respectively. Trp and 5-HIAA were measured by a fluorescence detector with an excitation wavelength of 295 nm and an emission wavelength of 340 nm. This allowed the determination of Kyn/Cr, Kyna/Cr, Trp/Cr and 5-HIAA/Cr concentration ratios in a single run on the same urine sample. Good linear responses were found with correlation coefficient (r)>0.999 for all analytes within the concentration range of physiological level. The limit of detection of the developed method was: Cr, 0.0002 g/L; Kyn, 0.1 μmol/L; Kyna, 0.04 μmol/L; Trp, 0.02 μmol/L and 5-HIAA, 0.01 μmol/L. Recoveries from spiked human urine were: Cr, 93.0-106.4%; Kyn, 97.9-106.9%; Kyna, 98.5-105.6%; Trp, 96.7-105.2% and 5-HIAA, 96.1-99.7%. CVs of repeatability and intermediate precision of all analytes were less than 5%. This method has been applied to the analysis of urine samples from normal subjects.
Journal of chromatography. B, Analytical technologies in the biomedical and life sciences 07/2011; 879(26):2720-5. · 2.78 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: TIGAR expression resulted in down-regulation of glycolysis, reduction of intracellular levels of reactive oxygen species, and protection from apoptosis. Despite biological importance, its promoter has not yet been characterized. In this study, we characterized that transcription factor SP1 plays a pivotal role for basal activity of TIGAR promoter. By 5'RACE, the transcription start site was identified locating at 134 bp upstream of the translation initiation site. Different portions of 5'-flanking and 5'-untranslated regions were fused to a luciferase reporter gene to create reporter plasmids, and constructs were transiently transfected into HepG2, Bel-7402, and Smmc-7721 cell lines for luciferase analysis. A minimal region -56/-4 bearing a SP1-binding site was characterized and plays a vital role. Data from electrophoretic mobility shift assay and chromatin immunoprecipitation showed that SP1 can interact with the SP1-binding site within TIGAR promoter in vitro and in vivo. Conclusively, SPl is indispensable for basal activity of TIGAR promoter.
Molecular and Cellular Biochemistry 07/2011; 359(1-2):17-23. · 2.06 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: We explored the role of the C-160A single-nucleotide polymorphism (SNP) of CDH1 in susceptibility to gastric cancer through a systematic review and meta-analysis. Fourteen studies were included, the original groups collapsed, and re-grouped in accordance with the most appropriate genetic model. Potential sources of heterogeneity were sought out via subgroup analyses and sensitivity analyses, and publication biases were estimated. No significant association of C-160A was found with the overall risk of developing gastric cancer, but the apparently opposite tendency was noted between Caucasians and Asians, and a statistically significant association was found among Asians. The seemingly opposite tendency of associations was also seen between noncardia and cardia types or between sporadic diffuse and intestinal types of gastric cancer, but no statistically significant findings were noted. Genotyping techniques, sample size, quality appraisal scores, or article publication time did not constitute the source of heterogeneity across studies; and no publication biases were found in our meta-analysis.
DNA and cell biology 05/2011; 30(11):937-45. · 2.28 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: CD166/ALCAM plays an important role in tumor aggression and progression as well as protecting cancer cells against apoptosis and autophagy. However, the mechanism by which pro-cell death signals control CD166 expression remains unclear. Here we show that following serum deprivation (SD), upregulation of CD166 protein is shorter than that of CD166 mRNA. Molecular analysis revealed both CD166 and miR-9-1 as two novel NF-κB target genes in hepatoma cells. In vivo activation and translocation of the NF-κB P50/P65 hetero-dimer into the nucleus following the phosphorylation and accompanied degradation of its inhibitor, IκBα, contributes to efficient transcription of both genes following SD. We show that following serum starvation, delayed up-regulation of miR-9 represses translation of CD166 protein through its target sites in the 3'-UTR of CD166 mRNA. We also propose that miR-9 promotes cell migration largely due to inhibition of CD166. Collectively, the study elucidates a novel negative auto-regulatory loop in which NF-κB mediates differential regulation of CD166 after SD.
Nucleic Acids Research 05/2011; 39(15):6440-55. · 8.03 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: There is a growing evidence that regucalcin (RGN) plays a multifunctional role in liver cancer cells. Previous reports showed that the presence of phorbol 12-myristate 13-acetate (PMA) caused a significant increase in RGN mRNA expression and promoter activity in rat hepatoma cells. In this study, we confirmed that human RGN is also up-regulated by PMA treatment independent of translation, and we identified the mechanism by which PMA up-regulates the expression of human RGN via driving SP1 away from a SP1 motif located within -188/-180 of the promoter in HepG2 cells. Overexpression of SP1 dramatically reduces PMA-induced up-regulation of both internal expression of mRNA and promoter activity, whereas knockdown of SP1 has the opposite effect. Therefore, the present study delineates the fundamental elements in the promoter which will be helpful in the future studies on the regulation of RGN expression in liver cancer.
Molecular and Cellular Biochemistry 04/2011; 355(1-2):9-15. · 2.06 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: To investigate the relationship between polymorphism of IL-1beta gene 31T/C and chronic rhinosinusitis.
One hundred and twenty-three patients with chronic rhinosinusitis and 239 healthy controls were collected to determine the genotypes by polymerase chain reaction-restriction fragment length polymorphism.
There was significant difference in genotype and allelic frequencies between the CRS and control group (P < 0.05). -31CC genotype was an independent risk factor with CRS (P < 0.05, OR = 1.639). There was no significant difference in TIgE and ECP among these genotypes (P > 0.05).
IL-1beta gene 31CC genotype may be an independent risk factor with chronic rhinosinusitis.
Lin chuang er bi yan hou ke za zhi = Journal of clinical otorhinolaryngology 03/2011; 25(5):197-200.
-
[show abstract]
[hide abstract]
ABSTRACT: The authors performed a systematic review and meta-analysis of associations of the x-ray repair cross-complementing 1 gene (XRCC1) single nucleotide polymorphisms (SNPs) Arg194Trp, Arg280His, and Arg399Gln with gastric cancer risk, based on eligible studies retrieved from electronic databases for the period January 2000-December 2009. Ultimately, 12, 6, and 3 studies were found to be eligible for meta-analyses of Arg399Gln, Arg194Trp, and Arg280His, respectively. Regrouping was adopted in accordance with the most probably appropriate genetic models. Potential sources of heterogeneity were sought out. For overall gastric cancer, the pooled odds ratios for Arg399Gln, Arg194Trp, and Arg280His were 1.04 (95% confidence interval (CI): 0.90, 1.20; P = 0.572), 0.83 (95% CI: 0.68, 1.01; P = 0.059), and 1.18 (95% CI: 0.92, 1.50; P = 0.194), respectively. After stratification of the Arg399Gln SNP data by anatomic type (cardia vs. noncardia), the pooled odds ratio was 1.07 (95% CI: 0.84, 1.37; P = 0.568). The authors conclude that the 3 SNPs evaluated are not associated with risk of gastric cancer. The Arg399Gln SNP is not associated with the cardia type of gastric cancer. Evidently, the heterogeneity regarding the Arg399Gln SNP across studies is not explained by ethnicity, genotyping technique, sample size, or date of publication.
American journal of epidemiology 02/2011; 173(4):363-75. · 5.59 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: Vascular endothelial growth factor (VEGF) plays a key role in the development of cerebral infarction as a major mediator of angiogenesis. The aim of this study was to investigate whether the VEGF gene polymorphisms were associated with the risks of acute cerebral infarction.
We examined the distribution of three single nucleotide polymorphisms (SNPs), -1154G/A, 936C/T and -2578C/A, in the promoter and coding region of the VEGF gene in DNA samples from 147 Chinese patients with acute cerebral infarction and 131 control subjects.
There was no significant difference in allele and genotype distributions of -1154G/A, 936C/T and -2578C/A with the risk of acute cerebral infarction when compared with controls. However, haplotype analysis from the above-mentioned three polymorphisms showed that haplotype ACC was significantly lower in patients with acute cerebral infarction (0.020) than in controls (0.054) (p = 0.034).
These data suggested that the -1154/, 936/ and -2578/ ACC haplotype was associated with the risk of acute cerebral infarction with an OR of 0.361, and it may reduce the risk of acute cerebral infarction through the regulation of VEGF expression.
European Neurology 01/2011; 66(1):47-52. · 1.81 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: RAB25 plays an important role in tumor progression and aggressiveness; altered RAB25 expression may cause human cancer. As the underlying mechanism of RAB25-mediated carcinogenesis in various tumor types progressively comes to light, RAB25 is expected to represent a novel therapeutic target. However, the regulation of RAB25 expression per se has not yet been described. Here we have firstly identified and characterized the human RAB25 promoter. Using PCR-based chromatin accessibility and chromatin immunoprecipitation (ChIP) assays, an open chromatin conformation (-173/+17) was detected around the transcription start site of the RAB25 gene. Deletion constructs of the 5' flanking region were fused to a luciferase reporter gene. After transient transfection in gastric cancer cell line AGS, a CRE (-67/-58) binding CREB was identified in the core promoter region. Electrophoretic mobility shift (EMSA) and ChIP assays demonstrated that CREB binds to the core promoter. Deletion of CREB consensus sequence resulted in the total loss of the promoter activity. Moreover, we have also found forskolin, PKA activator, could enhance open chromatin accessibility, by which to expose the CRE and facilitate phosphorylation of CREB, which in turn recruits co-factor CBP and Brg I and then results in a more open chromatin configuration associated with local histone modification, finally heightening RAB25 expression and strengthening its promoter activity. Therefore, the present study delineates the fundamental elements of a core promoter structure that will be helpful for future studies regarding the regulation of RAB25 gene.
The international journal of biochemistry & cell biology 11/2010; 43(3):348-57. · 4.89 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: We aimed to explore the role of interleukin (IL)-1B cluster gene polymorphisms at positions -511, -31, and +3954 and the receptor IL-1RN variable number tandem repeat polymorphisms in the susceptibility to gastric carcinoma through a systematic review and meta-analysis.
Each initially included article was scored for quality appraisal. The desirable data were extracted and registered into databases. Studies that deviated from Hardy-Weinberg equilibrium were excluded. Eighteen studies were ultimately eligible for the meta-analysis of IL1B-511, 21 studies for IL1B-31, 10 studies for IL1B+3954, and 20 studies for IL1RN variable number tandem repeat genetic polymorphisms, respectively. Original groups were collapsed and re-grouping was adopted in line with the most probably appropriate genetic models. Potential sources of heterogeneity were sought out via stratification and sensitivity analyses, and biases across studies were estimated.
The pooled odds ratios (95% confidence intervals, P-value) associated with IL-1B -511 T carriers versus CC genotypes and with RN *2 carriers versus L/L were 1.23 (1.04-1.45, P = 0.015) and 1.26 (1.06-1.51, P = 0.010), respectively, for overall gastric carcinoma; 1.31 (1.04-1.64, P = 0.020) and 1.47 (1.21-1.79, P = 0.000), respectively, for non-cardia gastric cancer; 1.55 (1.05-2.28, P = 0.026) and 1.66 (1.23-2.25, P = 0.001), respectively, for intestinal type gastric carcinoma; and 1.33 (1.04-1.71, P = 0.023) and 1.31 (1.07-1.61, P = 0.010), respectively, in Caucasians for overall gastric carcinoma. The pooled odds ratio (95% confidence interval, P-value) regarding IL-1B-31 CC plus TT versus CT was 0.73 (0.60-0.89, P = 0.002) for intestinal type gastric carcinoma. Genotyping methods and publication time could constitute the sources of heterogeneity across studies. Publication biases were not found.
IL-1B -511 T allele and IL-1 RN *2 VNTR are significantly associated with an increased risk of developing gastric carcinoma and even more significantly with non-cardia gastric carcinoma or with intestinal-type gastric carcinoma. Both are significantly associated with an increased risk of developing gastric carcinoma among Caucasians, but not among Asians or Hispanics.
Journal of Gastroenterology and Hepatology 10/2010; 25(10):1604-17. · 2.87 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: Long non-coding RNA (lncRNA), highly up-regulated in liver cancer (HULC) plays an important role in tumorigenesis. Depletion of HULC resulted in a significant deregulation of several genes involved in liver cancer. Although up-regulation of HULC expression in hepatocellular carcinoma has been reported, the molecular mechanisms remain unknown. In this study, we used in vivo and in vitro approaches to characterize cancer-dependent alterations in the chromatin organization and find a CREB binding site (encompassing from -67 to -53 nt) in the core promoter. Besides, we also provided evidence that PKA pathway may involved in up-regulation of HULC. Furthermore, we demonstrated HULC may act as an endogenous 'sponge', which down-regulates a series of microRNAs (miRNAs) activities, including miR-372. Inhibition of miR-372 leads to reducing translational repression of its target gene, PRKACB, which in turn induces phosphorylation of CREB. Over-expression of miR-372 decreases the association of CREB with the proximal promoter, followed by the dissociation of P300, resulting in a change of the histone 'code', such as in deacetylation and methylation. The study elucidates that fine tuning of HULC expression is part of an auto-regulatory loop in which it's inhibitory to expression and activity of miR-372 allows lncRNA up-regulated expression in liver cancer.
Nucleic Acids Research 09/2010; 38(16):5366-83. · 8.03 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: CD151 plays an important role in liver cancer metastasis. The mechanism on how CD151 is expressed remains unclear. Here we have identified SP1 is a protein functioning in constitutive activation of CD151. Applying a PCR-based chromatin accessibility assay, an open chromatin conformation was discovered localized around the transcription start site of the CD151 gene. Deletion constructs of the 5' flanking region were fused to a luciferase reporter gene. After transient transfection in HepG2 and Hep3B cells, a minimal region -171/-53 bearing three SP1-binding sites was identified as the core promoter. Results obtained from electrophoretic mobility shift and chromatin immunoprecipitation assays demonstrated that SP1 is bound to the core promoter. Deletion of SP1 consensus sequence resulted in the total loss of the promoter activity. Moreover, knockdown of SP1 reduced both CD151 promoter activity and chromatin accessibility. Conclusively, SP1 is pivotal to CD151 transcription partly via the construction of a local open chromatin configuration across the promoter.
Biochemical and Biophysical Research Communications 02/2010; 393(2):291-6. · 2.48 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: Pancreatic carcinoma is one of the most aggressive malignancies and carries the most dismal prognoses of all cancers. A better understanding of the genes involving in tumor development may allow us to tackle this rapidly progressive disease. The Net gene belongs to the ternary complex transcription factor (TCF) family and is regulated by the Ras/mitogen-activated protein kinase-signaling pathway. Under basal conditions, Net shows strong repressing function on transcription of proto-oncogene gene c-fos. Moreover, the lower expression of Net has been noted in some carcinoma cells, such as cervical cancer. To study the effect of Net on c-fos expression and its potential role in the growth of pancreatic carcinoma, we developed a recombinant plasmid, a pEGFP-N1-Net, which codes for Net-EGFP fusion proteins, and stably transfected it into BxPC-3 human pancreatic carcinoma cells. Using stable transformants, we were able to show that overexpression of Net decreased the expression of c-fos and inhibited pancreatic cancer cell proliferation. Cell cycle analysis demonstrated that Net overexpression inhibited cell cycle progression. These findings suggested that loss of Net repression could augment c-fos expression and further trigger neoplastic cell proliferation, which was involved in the pathogenesis of pancreatic cancer. Therefore, Net might be a potential target for the treatment of c-fos-positive pancreatic cancer.
The Tohoku Journal of Experimental Medicine 11/2008; 216(2):139-47. · 1.24 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: To investigate the association of restricted usage of repertoire of T cell receptor V beta (TCR V beta) with asthma.
In 36 Chinese asthmatics, peripheral blood TCR V beta was studied by means of fluorescein-labeled RT-PCR as well as genescan and genotype software analysis. The clonality of the predominant usage T cell receptors was analyzed by denaturing gel electrophoresis and single strand conformation polymorphism (SSCP) by using genescan analysis (with 377 ABI DNA sequencer).
The number of cases predominantly using TCRV beta 8 gene families in asthmatics and those allergy to house dust mite (HDM) was significantly higher than that of normal controls (P = 0.0230, 0.0147), and so the TCR V beta 5.1 gene family for asthmatics allergic to HDM (P = 0.0186). It is remarkable-that only two cases in 36 asthmatics were allergic to ragweed and both of them predominantly used TCR V beta 1 gene families. The TCR V beta gene families predominantly used in asthmatics showed polyclonal expression in all normal controls and most asthmatics, but 5 asthmatics showed oligoclonal expression of TCR V beta 8 gene families.
TCRV beta 8 and TCR V beta 5.1 gene families may be associated with allergy to HDM in asthmatics. TCR V beta gene families in asthmatic peripheral blood showed oligoclonal expression tendency.
Zhonghua jie he he hu xi za zhi = Zhonghua jiehe he huxi zazhi = Chinese journal of tuberculosis and respiratory diseases 03/2002; 25(2):78-80.
