RNA-seq Analysis of Differential Gene Expression in Obese Compared with Non-Obese Breast Cancer Patients
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA626358 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR11567100.fastq.gz | Fastqsanger.gz | |||
| SRR11567101.fastq.gz | Fastqsanger.gz | |||
| SRR11567102.fastq.gz | Fastqsanger.gz | |||
| SRR11567103.fastq.gz | Fastqsanger.gz | |||
| SRR11567104.fastq.gz | Fastqsanger.gz |
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Project description:Breast cancer (BC), the most common malignant tumor type, ranked top in incidence with high prevalence and mortality among females worldwide. Obesity poses a serious public health issue worldwide, it consider as one of BC risk factors. Obesity has profound effects on cancer cell transcriptome that can affect the outcome of cancer therapy. The information regarding the potential effects of obesity on BC transcriptome to identify novel transcripts biomarker and pathways related to disease progression are still elusive. Therefore, the RNA-seq analysis was performed to investigate the whole blood differential epressed genes profile in the blood liquid biopsy of obese compared with non-obese BC patients to provide a better understanding of the biological status and shed new insights into potential molecular mechanisms interaction and biomarkers in the relationship between obesity and BC.
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Project description:We aimed to characterize genetic alterations in PWS using whole genome microarrays. We performed mRNA expression microarray analysis using RNA isolated from whole blood of 25 PWS patients and 25 age-matched controls.. After preprocessing the data to reduce heterogeneity, differentially expressed genes (DEGs) between groups were identified using a linear regression model package. Reactome pathway analysis was performed for upregulated and downregulated genes using EnrichR. Correlations between gene expression levels and clinical factors were estimated using Spearman’s rank correlation coefficient. Of 21,488 probes examined in the microarray analysis, 4,156 were detected. Fifty-two genes had different expression levels in children with PWS compared with healthy controls (36 genes upregulated and 16 downregulated). Twelve genes were upregulated and 13 were downregulated in obese PWS patients compared with normal-weight PWS (NW-PWS) patients. The C-Type Lectin Domain Family 4 Member D (CLEC4D) was upregulated in both PWS (vs. control) and obese-PWS (vs. NW-PWS) patients, and CLEC4D expression was also correlated with body mass index-standard deviation score in PWS patients. Among the genes upregulated in obese PWS vs. NW-PWS, Annexin A3 (ANXA3), Potassium Inwardly Rectifying Channel Subfamily J Member 15 (KCNJ15), and Selenium Binding Protein 1 (SELENBP1) were upregulated in obese-control vs. NW-control. Gene Ontology analysis revealed that upregulated DEGs were significantly enriched in biological processes, including pathways involved in myeloid dendritic cell activation associated with CLEC4D.This study revealed differences in gene expression between obese and NW-PWS patients. The regulation of macrophage infiltration by CLEC4D suggests a possible mechanism associated with obesity-related complications in PWS.
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Project description:PWS gene expression profiling of obese and non-obese patients
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Project description:Objective: The etiology of PCOS is mostly unknown. Existing data support both genetic and environmental factors in its pathogenesis. Design: Prospective case - control study. Setting: University Hospital. Patients: 25 patients undergoing IVF-ICSI treatment. Intervention: Genome-wide oligonucleotide microarray technology was used to study differential gene-expression patterns of cultured human cumulus cells from IVF patients divided into 4 groups according to disease state (PCOS vs. Control) and BMI (Obese vs. Lean). Results: Two differential PCOS gene expression profiles were established: Lean-Type was formed by comparing PCOS lean (PL) vs. non-PCOS lean (NL) individuals; Obese-Type was formed by comparing PCOS obese (PO) vs. non-PCOS (NO) obese patients. Conclusions: Different molecular pathways are associated with PCOS in Lean and Obese individuals, as demonstrated by gene expression profiling of cumulus cells. Our findings provide insights into the molecular pathogenesis of PCOS. We used microarrays to study the gene expression of human cultured cumulus cells. We compared the genes expression of lean PCOS, Obese PCOS, lean controls and obese controls. Different molecular pathways are associated with PCOS in Lean and Obese patients. Keywords: disease state analysis
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Project description:Nonconverters exhibit differential transcriptional signatures compared to converters.
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Project description:Background/Objectives: Obese subjects have increased number of enlarged fat cells which are reduced in size but not number in post-obesity. We performed DNA methylation profiling in fat cells with the aim of identifying differentially methylated DNA sites (DMS) linked to adipose hyperplasia (many small fat cells) in post-obesity. Subjects/Methods: Genome-wide DNA methylation was analyzed in abdominal subcutaneous fat cells from 16 women examined two years after gastric bypass surgery at a post-obese state (BMI 26±2 kg/m2, mean±s.d.) and 14 never-obese women (BMI 25±2 kg/m2). Gene expression was analyzed in subcutaneous adipose tissue from 9 women in each group. In a secondary analysis, we examined DNA methylation and expression of adipogenesis genes in 15 and 11 obese women, respectively. Results: The average degree of DNA methylation of all analyzed CpG-sites was lower in fat cells from post-obese as compared to never-obese women (P=0.014). 8,504 CpG sites were differentially methylated in fat cells from post-obese versus never-obese women (false discovery rate 1%). DMS were under-represented in CpG-islands and surrounding shores. The 8,504 DMS mapped to 3,717 unique genes; these genes were over-represented in cell differentiation pathways. Notably, 27% of genes linked to adipogenesis (i.e. 35 of 130) displayed DMS (adjusted P=10−8) in post-obese versus never-obese women. Next, we explored DNA methylation and expression of genes linked to adipogenesis in more detail in adipose tissue samples. DMS annotated to adipogenesis genes were not accompanied by differential gene expression in post-obese compared to never-obese women. In contrast, adipogenesis genes displayed differential DNA methylation accompanied by altered expression in obese women, Conclusions: Global CpG hypomethylation and overrepresentation of DMS in adipogenesis genes in fat cells may contribute to adipose hyperplasia in post-obese women.
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Project description:Background/Objectives: Obese subjects have increased number of enlarged fat cells which are reduced in size but not number in post-obesity. We performed DNA methylation profiling in fat cells with the aim of identifying differentially methylated DNA sites (DMS) linked to adipose hyperplasia (many small fat cells) in post-obesity. Subjects/Methods: Genome-wide DNA methylation was analyzed in abdominal subcutaneous fat cells from 16 women examined two years after gastric bypass surgery at a post-obese state (BMI 26±2 kg/m2, mean±s.d.) and 14 never-obese women (BMI 25±2 kg/m2). Gene expression was analyzed in subcutaneous adipose tissue from 9 women in each group. In a secondary analysis, we examined DNA methylation and expression of adipogenesis genes in 15 and 11 obese women, respectively. Results: The average degree of DNA methylation of all analyzed CpG-sites was lower in fat cells from post-obese as compared to never-obese women (P=0.014). 8,504 CpG sites were differentially methylated in fat cells from post-obese versus never-obese women (false discovery rate 1%). DMS were under-represented in CpG-islands and surrounding shores. The 8,504 DMS mapped to 3,717 unique genes; these genes were over-represented in cell differentiation pathways. Notably, 27% of genes linked to adipogenesis (i.e. 35 of 130) displayed DMS (adjusted P=10−8) in post-obese versus never-obese women. Next, we explored DNA methylation and expression of genes linked to adipogenesis in more detail in adipose tissue samples. DMS annotated to adipogenesis genes were not accompanied by differential gene expression in post-obese compared to never-obese women. In contrast, adipogenesis genes displayed differential DNA methylation accompanied by altered expression in obese women, Conclusions: Global CpG hypomethylation and overrepresentation of DMS in adipogenesis genes in fat cells may contribute to adipose hyperplasia in post-obese women. Post obese=16, Control group=14.
2015-05-06 | E-GEOD-58622 | biostudies-arrayexpress
Project description:Characterization of genes associated with adipose tissue is key to understanding the pathogenesis of obesity and developing treatments for this disorder. Differential gene expression in the adipose tissue has been described in adulthood but none studies have been developed on childhood. The purpose of this study was to compare gene expression in omental adipose tissue from obese prepubertal and normal weight children. We selected 5 obese (BMI adjusted for age and sex z score >2) and 6 normal weight children. RNA was extracted from omental adipose tissue biopsies and cRNA was hybridizated on the human genome U133 Plus 2.0 Arrays (Affymetrix®). Microarray experiments were performed for each sample, and selected group of gene expression values were confirmed with real-time RT-PCR in 10 obese and 10 normal weigth prepubertal children. 1276 genes were found to be differentially expressed at P<0.05. Of those differential genes, 201 were upregulated (Fc>2) and 42 were downregulated (Fc<-2). Genes involved in metabolic and signalling pathways were altered in childhood obesity. Keywords: disease state analysis
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