THE ROLE OF DUSP22 (DUAL SPECIFICITY PHOSPHATASE 22) GENE EXPRESSION IN THE PROGNOSIS OF LOW GRADE LYMPHOMAS

2019 ◽  
Vol 37 ◽  
pp. 340-341 ◽  
Author(s):  
S. Paydas ◽  
E.K. Bagir ◽  
M. Ergin ◽  
G. Seydaoglu ◽  
A. Boz
Keyword(s):  
Gene Expression ◽  
Low Grade ◽  
Dual Specificity Phosphatase ◽  
Dual Specificity

scholarly journals Role of CL-100, a Dual Specificity Phosphatase, in Thrombin-induced Endothelial Cell Activation

2004 ◽  
Vol 279 (45) ◽  
pp. 46678-46685 ◽  
Author(s):  
Unni M. Chandrasekharan ◽  
Lin Yang ◽  
Alicia Walters ◽  
Philip Howe ◽  
Paul E. DiCorleto
Keyword(s):  
Endothelial Cell ◽  
Cell Activation ◽  
Endothelial Cell Activation ◽  
Dual Specificity Phosphatase ◽  
Dual Specificity

scholarly journals Intrauterine growth restriction affects hippocampal dual specificity phosphatase 5 gene expression and epigenetic characteristics

2011 ◽  
Vol 43 (20) ◽  
pp. 1160-1169 ◽  
Author(s):  
Xingrao Ke ◽  
Robert A. McKnight ◽  
Diana Caprau ◽  
Shannon O'Grady ◽  
Qi Fu ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cpg Methylation ◽  
Histone Code ◽  
Male Rat ◽  
Female Rat ◽  
Dual Specificity Phosphatase ◽  
Intrauterine Growth ◽  
Protein Levels ◽  
Dual Specificity ◽  
The Impact

Intrauterine growth retardation (IUGR) predisposes humans toward hippocampal morbidities, such as impaired learning and memory. Hippocampal dual specificity phosphatase 5 (DUSP5) may be involved in these morbidities because DUSP5 regulates extracellular signal-regulated kinase phosphorylation (Erk). In the rat, IUGR causes postnatal changes in hippocampal gene expression and epigenetic characteristics. However, the impact of IUGR upon hippocampal DUSP5 expression and epigenetic characteristics is not known. We therefore hypothesized that IUGR affects hippocampal 1) DUSP5 expression, DNA CpG methylation, and histone code, and 2) erk1/2 phosphorylation in a well-characterized rat model of IUGR. We found that IUGR significantly decreased DUSP5 expression in the day of life (DOL) 0 and 21 male rat, while decreasing only DUSP5 protein levels in the DOL21 female rat. Fluorescent in situ hybridization and immunohistochemistry analyses localized the changes in DUSP5 mRNA and protein, many of which occurred in the dentate gyrus. IUGR also caused sex-specific differences in DNA CpG methylation and histone code in two sites of the hippocampal DUSP5 gene, a 5′-flanking specificity protein-1 (SP1) site and exon 2. Finally, when IUGR decreased DUSP5 protein levels, Erk phosphorylation increased. We conclude that IUGR affects hippocampal DUSP5 expression and epigenetic characteristics in a sex-specific manner.

scholarly journals Downregulation of Dual-specificity phosphatase 9 promotes tumor progression and contributes to poor prognosis in colorectal cancer

2020 ◽  
Author(s):  
Zhaoyan Qiu ◽  
Ning Liang ◽  
Tao Sun ◽  
Hongyuan Xue ◽  
Tianyu Xie ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Functional Role ◽  
Cpg Island ◽  
Functional Study ◽  
Dual Specificity Phosphatase ◽  
Dual Specificity ◽  
Low Expression

Abstract Background Dual-specificity phosphatase 9 (DUSP9) belongs to the dual-specificity protein phosphatase subfamily. Recently, increasing attention has been paid on the role of DUSP9 in a variety of cancers. However, its functional role in tumor development is still unclear, especially in colorectal cancer (CRC). Methods The functional role of DUSP9 in inhibiting the progression of CRC was verified both in vivo and in vitro using colony formation assay, EdU incorporation assay, wound healing assay, nude mice xenograft model, and et al. RNA-seq was performed to assess the gene expression profiling in SW480 cells with DUSP9 stable knockdown and shControl cells. Bisulfite sequencing (BSE) was performed to reveal methylation status of CpG island in promoter of DUSP9. Results DUSP9 was significantly down regulated in tumor tissues compared with peritumor tissues. Moreover, low DUSP9 expression in CRC was closely associated with tumor size, depth of invasion and advanced TNM stage, indicating that DUSP9 may be involved in the progression of CRC. Kaplan–Meier survival analysis showed that the overall survival (OS) and recurrence-free survival (RFS) of patients with low expression of DUSP9 were significantly shorter than that of patients with high expression of DUSP9. Functional study revealed that DUSP9 inhibited tumor migration, invasion and metastasis both in vitro and in vivo . Mechanistically, low expression of DUSP9 in CRC was caused by the upregulation of miR-1246 and hypermethylation status of CpG island in promoter of DUSP9. Conclusion Our findings demonstrate that DUSP9 plays a critical role in the progression of CRC and therapeutic intervention to increase the expression or activity of DUSP9 may be a potential target for CRC treatment in the future.

scholarly journals Putative positive role of inflammatory genes in fat deposition supported by altered gene expression in purified human adipocytes and preadipocytes from lean and obese adipose tissues

2020 ◽  
Author(s):  
Sang-Hyeop Lee ◽  
Nak-Hyeon Choi ◽  
In-Uk Koh ◽  
Bong-Jo Kim ◽  
Song Lee ◽  
...  
Keyword(s):  
Gene Expression ◽  
Inflammatory Responses ◽  
Cell Types ◽  
Deposition Process ◽  
Fat Deposition ◽  
Low Grade ◽  
Positive Role ◽  
Inflammatory Genes ◽  
Altered Gene

Abstract BackgroundObesity is a chronic low-grade inflammatory disease that is generally characterized by enhanced inflammation in obese adipose tissue (AT). Here, we investigated alterations in gene expression between lean and obese conditions using mRNA-Seq data derived from human purified adipocytes (ACs) and preadipocytes (preACs). ResultsWe defined four classes of differentially expressed genes (DEGs) by comparing gene expression between 1) lean and obese ACs, 2) lean and obese preACs, 3) lean ACs and lean preACs, and 4) obese ACs and obese preACs. Based on an analysis of comparison 1, numerous canonical obesity-related genes, particularly inflammatory genes including IL6, TNF- and IL-1, i.e., the genes that are expected to be upregulated in obesity conditions, were found to be expressed at significantly lower levels in obese ACs than in lean ACs. In contrast, some inflammatory genes were found to be expressed at higher levels in obese preACs than lean preACs in the analysis of comparison 2. These two results indicate that (1) up-/downregulation of genes in ACs and preACs is inversely controlled during the fat deposition process and (2) preACs rather than ACs have increased inflammatory response genes in comparisons of lean and obese conditions for each of these cell types. Analysis of comparisons 3 and 4 showed that inflammatory gene classes were expressed at higher levels in differentiated ACs than undifferentiated preACs under both lean and obese conditions; however, the degree of upregulation was greater for lean than for obese conditions.ConclusionsTaken together, our analyses may suggest that lean fat differentiation involves even greater enhancement of inflammatory responses than does obese fat differentiation.

scholarly journals Obesity, Insulin Resistance, and Colorectal Cancer: Could miRNA Dysregulation Play a Role?

2019 ◽  
Vol 20 (12) ◽  
pp. 2922 ◽  
Author(s):  
Francesca Cirillo ◽  
Cecilia Catellani ◽  
Chiara Sartori ◽  
Pietro Lazzeroni ◽  
Sergio Amarri ◽  
...  
Keyword(s):  
Gene Expression ◽  
Colorectal Cancer ◽  
Insulin Resistance ◽  
Low Grade ◽  
Regulate Gene Expression ◽  
New Perspective ◽  
Obesity And Cancer ◽  
Low Grade Inflammation ◽  
Regulate Gene

Obesity is associated with insulin resistance and low-grade inflammation. Insulin resistance is a risk factor for cancer. A recent chapter in epigenetics is represented by microRNAs (miRNAs), which post-transcriptionally regulate gene expression. Dysregulated miRNA profiles have been associated with diseases including obesity and cancer. Herein we report dysregulated miRNAs in obesity both in animal models and in humans, and we also document dysregulated miRNAs in colorectal cancer (CRC), as example of an obesity-related cancer. Some of the described miRNAs are found to be similarly dysregulated both in obesity, insulin resistance (IR), and CRC. Thus, we present miRNAs as a potential molecular link between obesity and CRC onset and development, giving a new perspective on the role of miRNAs in obesity-associated cancers.

scholarly journals Putative positive role of inflammatory genes in fat deposition supported by altered gene expression in purified human adipocytes and preadipocytes from lean and obese adipose tissues

2020 ◽  
Author(s):  
Sang-Hyeop Lee ◽  
Nak-Hyeon Choi ◽  
In-Uk Koh ◽  
Bong-Jo Kim ◽  
Song Lee ◽  
...  
Keyword(s):  
Gene Expression ◽  
Inflammatory Responses ◽  
Low Grade ◽  
Transcriptome Data ◽  
Positive Role ◽  
Inflammatory Genes ◽  
Altered Gene Expression ◽  
Altered Gene ◽  
Geo Database

Abstract Background Obesity is a chronic low-grade inflammatory disease that is generally characterized by enhanced inflammation in obese adipose tissue (AT). Here, we investigated alterations in gene expression between lean and obese conditions using mRNA-Seq data derived from human purified adipocytes (ACs) and preadipocytes (preACs).Results Total mRNA-seq data were generated with 27 AC and 21 preAC samples purified from human visceral AT collected during resection surgery in cancer patients, where the samples were classified into lean and obese categories by BMI > 25 kg/m2. We defined four classes of differentially expressed genes (DEGs) by comparing gene expression between 1) lean and obese ACs, 2) lean and obese preACs, 3) lean ACs and lean preACs, and 4) obese ACs and obese preACs. Based on an analysis of comparison 1, numerous canonical obesity-related genes, particularly inflammatory genes including IL-6, TNF-a and IL-1b, i.e., the genes that are expected to be upregulated in obesity conditions, were found to be expressed at significantly lower levels in obese ACs than in lean ACs. In contrast, some inflammatory genes were found to be expressed at higher levels in obese preACs than lean preACs in the analysis of comparison 2. The analysis of comparisons 3 and 4 showed that inflammatory gene classes were expressed at higher levels in differentiated ACs than undifferentiated preACs under both lean and obese conditions; however, the degree of upregulation was significantly greater for lean than for obese conditions. We validated our observations using previously published microarray transcriptome data deposited in the GEO database (GSE80654).Conclusions Taken together, our analyses suggest that inflammatory genes are expressed at lower levels in obese ACs than in lean ACs because lean adipogenesis involves even greater enhancement of inflammatory responses than does obese adipogenesis.

scholarly journals Putative positive role of inflammatory genes in fat deposition supported by altered gene expression in purified human adipocytes and preadipocytes from lean and obese adipose tissues

2020 ◽  
Vol 18 (1) ◽  
Author(s):  
Sang-Hyeop Lee ◽  
Nak-Hyeon Choi ◽  
In-Uk Koh ◽  
Bong-Jo Kim ◽  
Song Lee ◽  
...  
Keyword(s):  
Gene Expression ◽  
Inflammatory Responses ◽  
Low Grade ◽  
Positive Role ◽  
Inflammatory Genes ◽  
Altered Gene Expression ◽  
Tnf Α ◽  
Altered Gene ◽  
Geo Database

Abstract Background Obesity is a chronic low-grade inflammatory disease that is generally characterized by enhanced inflammation in obese adipose tissue (AT). Here, we investigated alterations in gene expression between lean and obese conditions using mRNA-Seq data derived from human purified adipocytes (ACs) and preadipocytes (preACs). Results Total mRNA-seq data were generated with 27 AC and 21 preAC samples purified from human visceral AT collected during resection surgery in cancer patients, where the samples were classified into lean and obese categories by BMI > 25 kg/m2. We defined four classes of differentially expressed genes (DEGs) by comparing gene expression between (1) lean and obese ACs, (2) lean and obese preACs, (3) lean ACs and lean preACs, and 4) obese ACs and obese preACs. Based on an analysis of comparison 1, numerous canonical obesity-related genes, particularly inflammatory genes including IL-6, TNF-α and IL-1β, i.e., the genes that are expected to be upregulated in obesity conditions, were found to be expressed at significantly lower levels in obese ACs than in lean ACs. In contrast, some inflammatory genes were found to be expressed at higher levels in obese preACs than lean preACs in the analysis of comparison 2. The analysis of comparisons 3 and 4 showed that inflammatory gene classes were expressed at higher levels in differentiated ACs than undifferentiated preACs under both lean and obese conditions; however, the degree of upregulation was significantly greater for lean than for obese conditions. We validated our observations using previously published microarray transcriptome data deposited in the GEO database (GSE80654). Conclusions Taken together, our analyses suggest that inflammatory genes are expressed at lower levels in obese ACs than in lean ACs because lean adipogenesis involves even greater enhancement of inflammatory responses than does obese adipogenesis.

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