Increased plasma matrix metalloproteinase 1 is associated with the presence of esophageal squamous cell carcinoma
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE70409 | GEO | 2015/07/01
SECONDARY ACCESSION(S): PRJNA288571
REPOSITORIES: GEO
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Project description:Esophageal squamous cell carcinoma (ESCC) patients are usually diagnosed at late stages, prohibiting the chance of surgical cure. The obstacle partly comes from the lack of molecular markers for early detection. Moreover, there is no consensus about endoscopic surveillance for ESCC. This study aimed to identify noninvasive markers for ESCC detection. By microarray-based screening of 17 pairs of human ESCC specimens, we identified that secreted protein matrix metalloproteinase-1 (MMP1) may be associated with the presence of ESCC. The tumor and adjacent normal tissues were obtained from 17 male ESCC patients who underwent total esophagectomy without previous cancer treatment at Kaohsiung Medical University Hospital (KMUH)
2015-07-01 | E-GEOD-70409 | biostudies-arrayexpress
Project description:The incomplete surgical resection of invasive non-functional pituitary adenomas (iNFPAs) carries the increased risk of complications and requires adjuvant radiotherapy and medications. Thus, the molecular mechanisms and markers of invasiveness must be identified to guide the management of NFPA patients. This study explores the proteomic and transcriptomic variations of invasive and non-invasive NFPAs and other types of pituitary adenomas and evaluates the genetic markers in the exosome related to iNFPAs. The exosome from invasive and non-invasive NFPAs, prolactinomas (PRLs), growth hormone–secreting adenomas (GHs), adrenocorticotropic hormone-secreting adenomas (ACTHs), and normal pituitary tissue were analyzed. We confirmed that elevated matrix metalloproteinase-1 (MMP1) expression and its production in the exosome (exo-MMP1) are correlated with the invasive characteristics of NFPA. To investigate the molecular mechanism underlying the role of exo-MMP1 in invasiveness, we analyzed the effects of MMP1 on cell migration, cell growth and tumor angiogenesis. After transfection of MMP1 or a shRNA expression vector into NFPA cells, we obtained the associated exosome and observed that the altered expression and production of MMP1 in the exosome was significantly synchronized with the transduction of NFPA cells. In addition, the enrichment of MMP1 in the exosome promoted cell migration, cell growth and tumor angiogenesis via protease-activated receptor-1 (PAR1) signaling in recipient cells. Thus, these data demonstrate that MMP1 plays an important role in tumor invasion and angiogenesis and show that an exosome-mediated regulatory pathway for MMP1 may represent a target for therapeutic treatment.
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Project description:Primary sclerosing cholangitis (PSC) is a chronic liver disease characterized by biliary strictures, cholestasis, and an increased risk of cholangiocarcinoma (CCA). Here, we have used label-free quantitative proteomics to analyze serum and bile samples from non-PSC controls and PSC patients, as well as from PSC patients divided into groups according to endoscopic retrograde cholangiography score (with a score of >4 indicating advanced disease) and presence or absence of biliary dysplasia/CCA. Further analyses subsequently identified multiple candidates of new noninvasive serum markers for the diagnosis of PSC, as well as new markers for the prediction of the risk of disease progression and biliary neoplasia for patients already diagnosed with PSC.
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Project description:Recently, it was shown that the Bmp antagonist Noggin could strongly induce cardiomyocyte differentiation by transient treatment of undifferentiated ES cells. In order to determine how Noggin may induce cardiac differentiation, we compared differentially expressed genes during Noggin treatment of ES cells using microarray analysis and found that matrix metalloproteinase (Mmp)-3 is the only gene whose expression is increased by Noggin treatment. Keywords: embryonic stem cells, cardiac differentiation, matrix metalloproteinase-3, Noggin
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Project description:Aberrant DNA hypermethylation of CpG islands occurs frequently throughout the genome in human colorectal cancer (CRC). A genome-scale DNA hypermethylation analysis technique using plasma is attractive for the noninvasive early detection of CRC. The methylated CpG tandems amplification and sequencing (MCTA-Seq) method was applied to plasma samples from 147 CRC patients and 134 controls in which 5 from the CRC patients and 2 from the control subjects failed to pass a quality control value and were excluded from further analysis. The capacity of the method for discriminating CRC and hepatocellular carcinoma (HCC) was assessed. We identified many DNA methylation markers including known (e.g., SEPT9 and IKZF1) and novel (e.g., EMBP1, KCNQ5 and CHST11) CpG islands for detecting CRC in blood. A panel of 80 markers significantly discriminated early stage CRC and controls with a sensitivity of 78% and a specificity of 90%. This method can efficiently distinguish between early stage CRC and HCC. MCTA-Seq is a promising method for the noninvasive detection of CRC that also shows great potential for identifying the tissue of origin of cancer.
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Project description:A proportion of superficial esophageal squamous cell carcinoma, a type of less invasive esophageal squamous cell carcinoma (ESCC), would have metastasis after esophagectomy or endoscopic resection with poor prognosis. The purpose of this study was to discover the whole-genome copy number alteration (CNA) profiles of superficial ESCC and compare the CNAs of superficial ESCC patients with and without metastasis after surgery. Thirty eight superficial ESCC cases, including 19 cases with metastasis and 19 cases without metastasis within 5 years after surgery, were analyzed CNAs by Affymetrix OncoScan™ FFPE Assay. A 39-gene signature was initially constructed to identify high risk of metastasis in superficial ESCC patients. In addition, amplification of 11q13.3 (FGF4) and deletion of 9p21.3 (CDKN2A) were identified as recurrent CNAs across all 38 superficial ESCC cases. And amplifications of 3p26.33 (SOX2-OT), 8q24.21 (MYC), 14q21.1 (FOXA1) and deletion of 3p12.1 (GBE1) were identified as recurrent CNAs among metastasis cases only. Our study provided a 39-gene signature tool to identified high risk metastasis in superficial ESCC and suggested that amplifications of SOX2-OT, MYC, FOXA1 genes and deletion of GBE1 gene might play a vital role in metastasis among superficial ESCC.
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Project description:Esophageal squamous cell carcinoma (ESCC) is an aggressive tumor with poor prognosis. Understanding molecular changes in ESCC should improve identification of risk factors in molecular subtypes and provide potential targets for early detection and therapy. To better characterize molecular changes in ESCC, we followed up a previous cDNA array study with additional discovery and confirmatory studies in new ESCC cases using alternative methods. We profiled global gene expression (Affymetrix U133A/B chip) for discovery and confirmation, and validated selected dysregulated genes with additional RNA (qRT-PCR, N=51) or protein studies (immunohistochemistry [IHC] of tumor tissue microarray [TMA], N=275).We also found genes associated with survival. The dysregulated genes should aid in identifying risk factors in ESCC, as well as potential targets for early detection, and outcome prediction and therapy. 53 ESCC samples and 53 matched normal samples were analyzed (samples AE43 and AE45 were not run on HG-U133B due to not having enough material). Contributors have chosen not to include the clinical phenotypes in their GEO submission.
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Project description:Noninvasive prenatal diagnosis currently used does not achieve desirable levels of sensitivity and specificity. Recently, fetal methylated DNA biomarkers in maternal whole blood have been explored for noninvasive prenatal detection. However, such efforts cover only chromosomal aneuploidy; fetal methylated DNA biomarkers for detecting single-gene disease remain to be discovered. To address this issue, we systematically screened significantly hypermethylated genes in fetal tissues compared with maternal blood for noninvasive prenatal diagnosis of various inherited diseases. First, Methylated-CpG island recovery assay combined with CpG island array was performed in four maternal peripheral bloods and their corresponding placental tissues. Subsequently, direct bisulfite sequencing and combined bisulfite restriction analysis (COBRA) were carried out to validate the reliability of methylation microarray analysis. As results, 310 significantly hypermethylated genes in fetal tissues were detected by microarray. Two of five randomly selected hypermethylated genes detected by microarray were confirmed to be hypermethylated in fetal tissue samples by direct bisulfite sequencing. All four randomly selected hypermethylated genes detected by microarray were confirmed to be hypermethylated in five independent amniotic fluid samples and five independent chorionic villus samples from 10 pregnant women by CORBA. In conclusions, We found a lot of hypermethylated genes and methylation sites in fetal tissues, some of which have great potential to be developed into molecular markers for noninvasive prenatal diagnosis of monogenic disorders. Further clinical study is warranted to confirm these findings. Paired experiments, placental tissues vs. maternal peripheral bloods. Biological replicates: 4 placental tissues and 4 correspoding maternal peripheral bloods.
2012-02-22 | E-GEOD-35997 | biostudies-arrayexpress
Project description:We aimed to investigate the diagnostic potential of tumor educated platelets in ESCC. In this study, seventy-one ESCC patients and eighty healthy individuals were enrolled and divided into training cohort (23 patients and 27 healthy individuals) and validation cohort (48 patients and 53 healthy individuals). Next-generation RNA sequencing was performed on platelets isolated from peripheral blood of all participants and a support vector machine/leave-one-out cross validation (SVM/LOOCV) approach was used for binary classification. A diagnostic signature composed of ARID1A, GTF2H2 and PRKRIR discriminated ESCC patients from healthy individuals with 91.3% sensitivity and 85.2% specificity in the training cohort and 87.5% sensitivity and 81.1% specificity in the validation cohort. The AUC was 0.924 (95% CI, 0.845–0.956) and 0.893 (95% CI, 0.821–0.966), respectively, in the training cohort and validation cohort. This 3-gene platelet RNA signature could effectively discriminate ESCC from healthy control. Our data highlighted the potential of tumor educated platelets for the noninvasive diagnosis of ESCC. Moreover, we found keratin and collagen protein families, and ECM-related pathways might be involved in tumor progression and metastasis of ESCC, which might provide insights to understand ESCC pathobiology and advance novel therapeutics.
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