Expression data of tumor and non-tumor samples from patients with esophageal cancer
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Grace Fu
PROVIDER: E-GEOD-33810 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:Tumor-associated macrophages (TAMs) are known to be involved in progression, angiogenesis and motility of various cancers. We have previously reported the association between increased number of infiltrating TAMs with tumor progression and poor prognosis in esophageal squamous cell carcinomas (ESCCs). To study roles of TAMs in ESCC, we first exposed peripheral blood monocytes (PBMo) derived macrophages from healthy volunteers to conditioned media of TE series human ESCC cell line (TECM) and confirmed the induction of expression of M2 macrophage marker, CD204, and protumorigenic factors, interleukin (IL)-10, VEGFA and MMPs. Next, we compared gene expression profile between PBMo-derived macrophages and PBMo-derived macrophages stimulated with TECM by cDNA microarray. Based on the result, we focused on growth differentiation factor 15 (GDF15) among highly expressed genes including IL-6, IL-8 and CXCL1. Immunohistochemical study on 70 cases of surgically resected ESCCs revealed that GDF15 was detected not only in macrophages but also in cancer cells. High expression of GDF15 in ESCCs was significantly correlated with more malignant phenotypes including lymph and blood vessel invasion, lymph node metastasis as well as clinical stages. Patients with high expression of GDF15 showed poor disease-free survival (p = 0.011) and overall survival (p = 0.041). Furthermore, we found that recombinant human GDF15 promote cell proliferation and phosphorylation of both Akt and Erk1/2 in ESCC cell lines in vitro. These results indicate that GDF15 is secreted by both TAMs and cancer cells in tumor microenvironment and is associated with aberrant growth and poor prognosis of human ESCC. We exposed PBMo-derived macrophages from healthy volunteers to TECM and observed their acquisition of TAM-like characters in this study. We further investigated specific cancer-associated gene expression profile in TECM induced TAM-like macrophages by cDNA microarray analysis.
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Project description:Signal transducer and activator of transcription 3 (STAT3) is altered in several epithelial cancers and represents a potential therapeutic target. Here, STAT3 expression, activity and cellular functions were examined in two main histotypes of esophageal carcinomas. In situ, immunohistochemistry for STAT3 and STAT3-Tyr705 phosphorylation (P-STAT3) in esophageal squamous cell carcinomas (ESCC) and Barrett’s adenocarcinomas (BAC) revealed similar STAT3 expression in ESCCs and BACs, but preferentially activated P-STAT3 in ESCCs. In vitro, strong STAT3 activation was seen by EGF-stimulation in OE21 (ESCC) cells, whilst OE33 (BAC) cells showed constitutive weak STAT3 activation. STAT3 knockdown significantly reduced cell proliferation of OE21 and OE33 cells and reduced cell migration in OE33, but not in OE21 cells. Transcriptome analysis identified STAT3-knockdown associated down-regulation of cell cycle processes and the selective down-regulation of cyclins and cyclin dependent kinaes associated genes in both OE21 and OE33 cells. Moreover, the transcriptome response showed changes in cell migration/invasion related genes that correlated with the associated phenotype measurements. This study demonstrates the importance of STAT3 expression and activation in esophageal carcinomas, whereby the extent differs between ESCCs and BACs. STAT3 knockdown significantly reduces cell proliferation in both types of esophageal cancer cells and inhibits migration in BAC cells. Thus, STAT3 may be further exploited as potential novel therapeutic target for esophageal cancers.
2013-06-16 | GSE47763 | GEO
Project description:Tumor-associated macrophages (TAMs) are known to be involved in progression, angiogenesis and motility of various cancers. We have previously reported the association between increased number of infiltrating TAMs with tumor progression and poor prognosis in esophageal squamous cell carcinomas (ESCCs). To study roles of TAMs in ESCC, we first exposed peripheral blood monocytes (PBMo) derived macrophages from healthy volunteers to conditioned media of TE series human ESCC cell line (TECM) and confirmed the induction of expression of M2 macrophage marker, CD204, and protumorigenic factors, interleukin (IL)-10, VEGFA and MMPs. Next, we compared gene expression profile between PBMo-derived macrophages and PBMo-derived macrophages stimulated with TECM by cDNA microarray. Based on the result, we focused on growth differentiation factor 15 (GDF15) among highly expressed genes including IL-6, IL-8 and CXCL1. Immunohistochemical study on 70 cases of surgically resected ESCCs revealed that GDF15 was detected not only in macrophages but also in cancer cells. High expression of GDF15 in ESCCs was significantly correlated with more malignant phenotypes including lymph and blood vessel invasion, lymph node metastasis as well as clinical stages. Patients with high expression of GDF15 showed poor disease-free survival (p = 0.011) and overall survival (p = 0.041). Furthermore, we found that recombinant human GDF15 promote cell proliferation and phosphorylation of both Akt and Erk1/2 in ESCC cell lines in vitro. These results indicate that GDF15 is secreted by both TAMs and cancer cells in tumor microenvironment and is associated with aberrant growth and poor prognosis of human ESCC.
2014-08-01 | GSE59948 | GEO
Project description:We used cDNA microarray to study the gene expression profile between the tumor and non-tumor tissue samples from patients with esophageal cancer
2011-11-19 | GSE33810 | GEO
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| PRJNA464348 | ENA
Project description:This SuperSeries is composed of the following subset Series: GSE37200: Gene expression profiling of Barrett’s esophageal tissues and esophageal adenocarcinoma specimens GSE37201: Gene expression profiling of esophageal adenocarcinoma Refer to individual Series
2012-04-10 | E-GEOD-37203 | biostudies-arrayexpress
Project description:Esophageal cancer is among the 10 most common malignancies and ranks as the 6th leading cause of death from cancer. It constitutes 7% of all gastrointestinal cancers and is one of the most lethal of all cancers. The large variation in the incidence of esophageal cancer in different geographic regions has often been thought to be due to variation in exposure to environmental factors; however, hereditary factors may also contribute to the variation in rates. A positive family history was found to be associated with an increased risk of esophageal cancer in several case-control and cohort studies in China. Familial aggregation also has been observed in Iran and Japan. The cancer data generated from six hospital based cancer registries in India under National Cancer Registry Programme (NCRP, Annual Report, 2003-2004) has revealed that the occurrence of esophageal cancer in Assam is highest in India. The aggregation of esophageal cancer in families is a long-observed and well-documented phenomenon in Assam of North-east part of India (AAR=32.6). In Assam high incidence of esophageal cancer with familial aggregation need investigation for etiology. The etiology of esophageal cancer in Northeast Indian population is different from other population at India due to wide variations in dietary habits or nutritional factors, tobacco chewing and alcohol habits. With in these high-risk regions, studies have shown a strong tendency toward familial aggregation, suggesting that genetic susceptibility, in conjunction with potential environmental exposures, may be involved in the etiology of esophageal cancer. Familial clustering of cancer has been one of the main avenues to the understanding of cancer etiology and the signal to the involvement of heritable genes. Familial clustering of cancer may be due to environmental factors shared by family members or due to shared genes. However, the familial aggregation of esophageal cancer among the population in northeast India may reflect the influence of environmental factors operating on individuals who are already genetically susceptible. Epidemiological studies indicate that tobacco smoking and alcohol consumption are the major factors for esophageal cancer, the role of genetic factors for familial aggregation has not been elucidated. In this study, tumor and matched normal tissue from esophageal squamous cell carcinoma patients with a family history of upper gastrointestinal cancer were analyzed using cDNA microarray containing 10,000genes to evaluate gene expression differences in esophageal squamous cell carcinoma patients with a family history of upper gastrointestinal cancer from a high- risk area in India. To identify alteration in genes and molecular functional pathways in esophageal cancer in a high incidence region of India where there is wide spread use of tobacco and betel quid with fermented areca nuts and familial aggregation cancer. Low RNA Input Fluorescent Linear Amplification Kit (Agilent, Santa Clara, CA) was used for labeling. Briefly, both first and second strand cDNA were synthesized by incubating 500ng of total RNA with 1.2ul of oligo dT-T7 Promoter Primer in nuclease-free water at 65 â¦C for 10 min followed by incubation with 4.0ul of 5à First strand buffer, 2ul of 0.1M DTT, 1 ul of 10mM dNTP mix, 1ul of 200 U/ul MMLV-RT, and 0.5ul of 40U/ul RNaseOUT, at 40 â¦C for 2 hour. Immediately following cDNA synthesis, the reaction mixture was incubated with 2.4 ul of 10 mM Cyanine-3-CTP or 2.4 ul of 10 mM Cyanine-5-CTP (Perkin-Elmer, Boston, MA), 20ul of 4X Transcription buffer, 8 ul of NTP mixture, 6 ul of 0.1M DTT, 0.5 ul of RNaseOUT, 0.6ul of Inorganic pyrophosphatase, 0.8 ul of T7 RNA polymerase, and 15.3ul of nuclease-free water at 40 â¦C for 2 hour. Qiagenâs RNeasy mini spin columns were used for purifying amplified aRNA samples. The quantity and specific activity of cRNA was determined by using NanoDrop ND-1000 UV-VIS Spectrophotometer version3.2.1. Samples with specific activity >8 were used for hybridization. 825ng of each Cyanine 3 or Cyanine 5 labeled cRNA in a volume of 41.8ul were combined with 11ul of 10x Blocking agent and 2.2ul of 25x Fragmentation buffer (Agilent), and incubated at 60deg C for 30 minutes in dark. The fragmented cRNA were mixed with 55ul of 2x Hybridization Buffer (Agilent). About 110ul of the resulting mixture was applied to the Microarray and hybridized at 65degC for 17 hours in an Agilent Microarray Hybridization Chamber (SureHyb: G2534A) with Hybridization Oven. After hybridization, slides were washed with Agilent Gene expression Wash Buffer I for 1 minute at room temperature followed by a 1 min wash with Agilent Gene expression Wash Buffer II for 37C. Slides were finally rinsed with Acetonitrile for cleaning up and drying. Microarrays were scanned on an Agilent scanner (G2565AA) at 100% laser power, 30% PMT.Data extraction was carried out with Agilent Feature Extraction software (version 9.1), and normalization was done using linear per array algorithm according to the manufacturerâs protocol. The data was analysed by GeneSpring GX and Biointerpreter software from Genotypic Technology, Bangalore. The differential expression was considered if the Log 2 mean of at least -1 for the down regulated genes and +1 for the upregulated genes. We considered only the genes that were reproducible from all replicates.
2010-06-25 | E-GEOD-10127 | biostudies-arrayexpress