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Liu H.,Harbin Medical University | Liu H.,Center for Infection and Genomics | Liu H.,University of Calgary | Yan Z.-Q.,Harbin Medical University | And 11 more authors.
Journal of Ovarian Research | Year: 2014

Background: Products of the SOX gene family play important roles in the life process. One of the members, SOX7, is associated with the development of a variety of cancers as a tumor suppression factor, but its relevance with ovarian cancer was unclear. In this study, we investigated the involvement of SOX7 in the progression and prognosis of epithelial ovarian cancer (EOC) and the involved mechanisms. Methods: Expression profiles in two independent microarray data sets were analyzed for SOX7 between malignant and normal tissues. The expression levels of SOX7 in EOC, borderline ovarian tumors and normal ovarian tissues were measured by immunohistochemistry. We also measured levels of COX2 and cyclin-D1 to examine their possible involvement in the same signal transduction pathway as SOX7. Results: The expression of SOX7 was significantly reduced in ovarian cancer tissues compared with normal controls, strongly indicating that SOX7 might be a negative regulator in the Wnt/β-catenin pathway in ovarian cancer. By immunohistochemistry staining, the protein expression of SOX7 showed a consistent trend with that of the gene expression microarray analysis. By contrast, the protein expression level of COX2 and cyclin-D1 increased as the tumor malignancy progressed, suggesting that SOX7 may function through the Wnt/β-catenin signaling pathway as a tumor suppressor. In comparison between the protein expression levels of SOX7 with pathological features of the cancer, we found that SOX7 was down-regulated mainly in serous cystadenocarcinoma and advanced stages of the cancers. Conclusions: The expression of SOX7 correlates with tumor progression as a tumor suppressor, possibly through the Wnt/β-catenin signaling pathway in ovarian cancers, suggesting that SOX7 may be a promising prognostic marker. © 2014 Liu et al.; licensee BioMed Central Ltd.


Jiao Y.,University of Tennessee Health Science Center | Jiao Y.,Mudanjiang Medical College | Chen H.,First Hospital of Qiqihaer City | Gu T.,University of Tennessee Health Science Center | And 4 more authors.
BMC Research Notes | Year: 2015

Background: Considerable progress has been made in illuminating the pathological events for systemic sclerosis (SSc)-related progressive lung fibrosis. The molecular events that lead to SSc-related progressive lung fibrosis need to be defined. Some important genes have been identified from a recent study in humans. We aim to construct and compare the similarities and differences of molecular pathways between SSc-related progressive lung fibrosis and normal lungs of humans and mice. Methods: We used the analytical approach of association of key genes in SSc-related progressive lung fibrosis. We first identified the probes for genes of SSc-related progressive lung fibrosis and analyzed the pathways in human lung using data generated by microarray. We then analyzed the gene pathways in mouse lung for similar sets of probes. Gene expression data from livers were used to compare with that in lung in both humans and mice. Results: Our analysis indicated that, in humans, the expression levels of genes for macrophage activation are more strongly associated with each other than that in mice. In both humans and mice, the associations of these genes are much greater in the lung than that in the liver. The association in gene expression between humans and mice are similar for IFN-regulated genes and profibrotic/Tgfβ-regulated genes. Conclusion: Our analysis reveals the differences and similarities of the network of key genes between humans and mice during the molecular processes that eventually lead to fibrosis in the lung. © 2015 Jiao et al.


Wang L.,University of Tennessee Health Science Center | Wang L.,Inner Mongolia University | Huang Y.,University of Tennessee Health Science Center | Jiao Y.,University of Tennessee Health Science Center | And 7 more authors.
Gene Expression | Year: 2013

The purpose of this study is to investigate whether expression profiles of alcoholism-relevant genes in different parts of the brain are correlated differently with those in the liver. Four experiments were conducted. First, we used gene expression profiles from five parts of the brain (striatum, prefrontal cortex, nucleus accumbens, hippocampus, and cerebellum) and from liver in a population of recombinant inbred mouse strains to examine the expression association of 10 alcoholism-relevant genes. Second, we conducted the same association analysis between brain structures and the lung. Third, using five randomly selected, nonalcoholism-relevant genes, we conducted the association analysis between brain and liver. Finally, we compared the expression of 10 alcoholism-relevant genes in hippocampus and cerebellum between an alcohol preference strain and a wild-type control. We observed a difference in correlation patterns in expression levels of 10 alcoholismrelevant genes between different parts of the brain with those of liver. We then examined the association of gene expression between alcohol dehydrogenases (Adh1, Adh2, Adh5, and Adh7) and different parts of the brain. The results were similar to those of the 10 genes. Then, we found that the association of those genes between brain structures and lung was different from that of liver. Next, we found that the association patterns of five alcoholism-nonrelevant genes were different from those of 10 alcoholism-relevant genes. Finally, we found that the expression level of 10 alcohol-relevant genes is influenced more in hippocampus than in cerebellum in the alcohol preference strain. Our results show that the expression of alcoholism-relevant genes in liver is differently associated with the expression of genes in different parts of the brain. Because different structural changes in different parts of the brain in alcoholism have been reported, it is important to investigate whether those structural differences in the brains of those with alcoholism are due to the difference in the associations of gene expression between genes in liver and in different parts of the brain. Copyright © 2013 Cognizant Comm. Corp.


Yan J.,University of Tennessee Health Science Center | Jiao Y.,University of Tennessee Health Science Center | Jiao Y.,Mudanjiang Medical College | Chen H.,First Hospital of Qiqihaer City | And 4 more authors.
Journal of Genetics and Genomics | Year: 2013

Previous studies have revealed the significance of cytokine interleukin 1 (IL-1) in the onset and progression of rheumatoid arthritis (RA). The precise molecular mechanisms related to IL-1 underlying RA is still elusive. We conducted a whole genome-wide transcriptomal comparison of wild-type (WT) and arthritis-prone IL-1 receptor antagonist (IL-1rn) deficient BALB/c mice to address this issue. To refine our search efforts, gene expression profiling was also performed on paired wild-type and arthritis-resistant IL-1rn deficient DBA/1 mice as internal controls when identifying causative arthritis candidate genes. Two hundred and fifteen transcripts were found to be dysregulated greater than or equal to 2-fold in the diseased mice. The altered transcriptome in BALB/c mice revealed increased myeloid cell activities and impaired lymphocyte functionality, suggesting dual regulatory effects of IL-1 hyperactivity on immunological changes associated with arthritis development. Phase-specific gene expression changes were identified, such as early increase and late decrease of heat shock protein coding genes. Moreover, common gene expression changes were also observed, especially the upregulation of paired Ig-like receptor A (Pira) in both early and late phases of arthritis. Real-time PCR was performed to validate the expression of Pira and an intervention experiment with a major histocompatibility complex (MHC) class I inhibitor (brefeldin A) was carried out to investigate the role of suppressing Pira activity. We conclude that global pattern changes of common and distinct gene expressions may represent novel opportunities for better control of RA through early diagnosis and development of alternative therapeutic strategies. © 2013.


Hu Y.-Z.,Harbin Medical University | Wang D.-H.,Harbin Medical University | Gong H.-D.,Harbin Medical University | Li G.-Z.,Harbin Medical University | And 4 more authors.
Chinese Journal of Cancer Prevention and Treatment | Year: 2013

OBJECTIVE: To investigate the relationship between the polymorphism of XRCC1 and MGMT and susceptibility to glioma in Han population northeastern China. METHODS: A hospital-based case-control study with glioma and none cancer or outpatients as a control group (matched for ages±5 years and sex) in Han population northeastern China was conducted to analyze XRCC1 polymorphism at Arg399Gln(included 366 glioma patients and 377 healthy controls) and MGMT polymorphism at Leu84Phe(included 543 glioma patients and 495 healthy controls), Ile143Val(included 369 glioma patients and 441 healthy controls). Genetyped by PCR-based restriction fragment length polymorphism(PCR-RFLP) techniques. RESULTS: The frequencies of 399Gln allele gene in the glioma patients was 0.35, which was significantly higher than that in controls 0.27(χ2=7.485, P=0.006). Compared with individuals with the Arg/Arg genetype, individuals with the Gln genotype, the Arg/Gln individual increased the glioma risk (OR=1.36, 95%CI=1.01-1.85, P=0.045); Gln/Gln individual increased the glioma risk(OR=1.83, 95%CI=1.10-3.05, P=0.019); Arg/Gln + Gln/Gln individual increased the glioma risk(OR =1.44, 95%CI=1.08-1.93, P=0.013); allele Gln individual increased the glioma risk(OR=1.36, 95%CI=1.09-1.69, P=0.006). The frequencies of 84Phe allele gene in the glioma patients was 0.16, which was significantly higher than that in controls 0.10(χ2=20.253, P<0.001). Compared with individuals with the Leu/Leu genetype, individuals with the Leu/Phe increased the glioma risk(OR =1.61, 95%CI=1.18-2.19, P=0.002); Phe/Phe individual increased the glioma risk(OR=4.16, 95%CI=1.68-10.30, P=0.001); Leu/Phe + Phe/Phe individual increased the glioma risk(OR=1.78, 95%CI=1.33-2.39, P<0.001); allele Phe individual increased the glioma risk(OR=1.83, 95%CI=1.40-2.38, P<0.001). The frequencies of 143Val allele gene in the glioma patients was 0.11, which was no evidence of an association in controls 0.10(χ2=0.242, P=0.623). Compared with individuals with the Ile/Ile genetype, individuals with the Ile/Val or Val/Val or Ile/Val + Val/Val and allele Val individual did not increase the glioma risk(P>0.05). CONCLUSIONS: The XRCC1 Arg399Gln and MGMT Leu84Phe polymorphism can add the risk to the occurrence of glioma in a Han population in northeastern China, which can elevate the occurrence of glioma. No significant correlation is found between MGMT gene polymorphism of Ile143Val and glioma.

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