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Articles by J Deng
Total Records ( 4 ) for J Deng
  J Deng , J Fujimoto , X. F Ye , T. Y Men , C. S Van Pelt , Y. L Chen , X. F Lin , H Kadara , Q Tao , D Lotan and R. Lotan
 

Mouse models can be useful for increasing the understanding of lung tumorigenesis and assessing the potential of chemopreventive agents. We explored the role of inflammation in lung tumor development in mice with knockout of the tumor suppressor Gprc5a. Examination of normal lung tissue and tumors from 51 Gprc5a+/+ (adenoma incidence, 9.8%; adenocarcinoma, 0%) and 38 Gprc5a–/– mice (adenoma, 63%; adenocarcinoma, 21%) revealed macrophage infiltration into lungs of 45% of the Gprc5a–/– mice and 8% of Gprc5a+/+ mice and the direct association of macrophages with 42% of adenomas and 88% of adenocarcinomas in the knockout mice. Gprc5a–/– mouse lungs contained higher constitutive levels of proinflammatory cytokines and chemokines and were more sensitive than lungs of Gprc5a+/+ mice to stimulation of NF-B activation by lipopolysaccharide in vivo. Studies with epithelial cells cultured from tracheas of Gprc5a–/– and Gprc5a+/+ mice revealed that Gprc5a loss is associated with increased cell proliferation, resistance to cell death in suspension, and increased basal, tumor necrosis factor –induced, and lipopolysaccharide-induced NF-B activation, which were reversed partially in Gprc5a–/– adenocarcinoma cells by reexpression of Gprc5a. Compared with Gprc5a+/+ cells, the Gprc5a–/– cells produced higher levels of chemokines and cytokines and their conditioned medium induced more extensive macrophage migration. Silencing Gprc5a and the p65 subunit of NF-B in Gprc5a+/+ and Gprc5a–/– cells, respectively, reversed these effects. Thus, Gprc5a loss enhances NF-B activation in lung epithelial cells, leading to increased autocrine and paracrine interactions, cell autonomy, and enhanced inflammation, which may synergize in the creation of a tumor-promoting microenvironment. Cancer Prev Res; 3(4); 424–37. ©2010 AACR.

  S. K Park , G Andreotti , A Rashid , J Chen , P. S Rosenberg , K Yu , J Olsen , Y. T Gao , J Deng , L. C Sakoda , M Zhang , M. C Shen , B. S Wang , T. Q Han , B. H Zhang , M Yeager , S. J Chanock and A. W. Hsing
 

Biliary tract cancer encompasses tumors of the gallbladder, bile duct and ampulla of Vater. Gallbladder cancer is more common in women, whereas bile duct cancer is more common in men, suggesting that sex hormones may play a role in the etiology of these cancers. The intracellular action of estrogens is regulated by the estrogen receptor (ESR); thus, we examined the role of common genetic variants in ESR genes on the risk of biliary tract cancers and stones in a population-based case–control study in Shanghai, China (411 cancer cases, 895 stone cases and 786 controls). We genotyped six single-nucleotide polymorphisms (SNPs), four in ESR1 (rs2234693, rs3841686, rs2228480 and rs1801132) and two in ESR2 (rs1256049 and rs4986938). In all participants, the ESR1 rs1801132 (P325P) G allele was associated with excess risks of bile duct [odds ratio (OR) = 1.7, 95% confidence interval (CI) 1.1–2.8] and ampulla of Vater cancers (OR = 2.1, 95% CI 0.9–4.9) compared with the CC genotype. The association with bile duct cancer was apparent among men (OR = 2.8, 95% CI 1.4–5.7) but not among women (P-heterogeneity = 0.01). Also, the ESR2 rs4986938 (38 bp 3' of STP) GG genotype was associated with a higher risk of bile duct cancer (OR = 3.3, 95% CI 1.3–8.7) compared with the AA genotype, although this estimate was based on a small number of subjects. None of the other SNPs examined was associated with biliary tract cancers or stones. False discovery rate-adjusted P-values were not significant (P > 0.1). No association was found for ESR1 haplotype based on four SNPs. These preliminary results suggest that variants in ESR genes could play a role in the etiology of biliary tract cancers, especially bile duct cancer in men.

  R Shoemaker , J Deng , W Wang and K. Zhang
 

In diploid mammalian genomes, parental alleles can exhibit different methylation patterns (allele-specific DNA methylation, ASM), which have been documented in a small number of cases except for the imprinted regions and X chromosomes in females. We carried out a chromosome-wide survey of ASM across 16 human pluripotent and adult cell lines using Illumina bisulfite sequencing. We applied the principle of linkage disequilibrium (LD) analysis to characterize the correlation of methylation between adjacent CpG sites on single DNA molecules, and also investigated the correlation between CpG methylation and single nucleotide polymorphisms (SNPs). We observed ASM on 23%~37% heterozygous SNPs in any given cell line. ASM is often cell-type-specific. Furthermore, we found that a significant fraction (38%~88%) of ASM regions is dependent on the presence of heterozygous SNPs in CpG dinucleotides that disrupt their methylation potential. This study identified distinct types of ASM across many cell types and suggests a potential role for CpG-SNP in connecting genetic variation with the epigenome.

  J Deng , X Liao , J Hu , X Leng , J Cheng and G. Zhao
 

In contrast to animal ferritin, relatively little information is available on phytoferritin. Black bean (Phaseolus vulgaris L.) has been consumed in many countries. In the present study, new ferritin from black bean seed was purified by two consecutive anion exchange and size exclusion chromatography. The apparent molecular mass of the native black bean seed ferritin (BSF) was found to be ~560 kDa by native PAGE analysis. N-terminal sequence, MALDI-TOF-MS and MS/MS analyses indicate that BSF and soybean seed ferritin (SSF) share very high identity in amino acid sequence. However, SDS–PAGE result indicates that BSF consists of 26.5 (H-1) and 28.0 kDa (H-2) subunits with a ratio of 2 : 1, while the ratio of these two subunits in SSF is 1 : 1. This result demonstrates that the two proteins have different subunit composition which might affect their activities in iron uptake and release. Indeed, at high iron flux, the initial rate of iron oxidative deposition in apoBSF is larger than that in apoSSF. On the contrary, the iron release from BSF is significantly slower than that from SSF. All these results indicate that phytoferritin might regulate the transit of iron into and out of the protein cavity by changing its subunit composition.

 
 
 
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