Molecular profiling of CML CD34+CD38- cells 6h and 24h post stimulation with conditioned media (CM) derived from either CXCL14 overexpressed NIH3 (NIH3-CXCL14) cells or control cells.
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE201122 | GEO | 2023/10/01
REPOSITORIES: GEO
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Project description:Molecular profiling of CML CD34+CD38- cells 6h and 24h post stimulation with conditioned media (CM) derived from either CXCL14 overexpressed NIH3 (NIH3-CXCL14) cells or control cells.
| PRJNA828522 | ENA
Project description:BACKGROUND: BCR-ABL1+ chronic myeloid leukemia (CML) is characterized by abnormal production of leukemic stem (LSC) and progenitor cells and their spread from the bone marrow into the blood resulting in extramedullary myeloproliferation. So far, little is known about specific markers and functions of LSC in CML. METHODS: We examined the phenotype and function of CD34+/CD38─/Lin─ CML LSC by a multi-parameter screen approach employing antibody-phenotyping, mRNA expression profiling, and functional studies, including LSC repopulation experiments in irradiated NOD-SCID-IL-2Rgamma-/- (NSG) mice, followed by marker-validation using diverse control-cohorts and follow-up samples of CML patients treated with imatinib. RESULTS: Of all LSC markers examined, dipeptidylpeptidase IV (DPPIV=CD26) was identified as specific and functionally relevant surface marker-enzyme on CD34+/CD38─ CML LSC. CD26 was not detected on normal CD34+/CD38─ stem cells or LSC in other hematopoietic malignancies. The percentage of CD26+ CML LSC decreased to undetectable levels during successful treatment with imatinib in all patients (p<0.001). Whereas the sorted CD26─ stem cells obtained from CML patients engrafted irradiated NSG mice with multilineage BCR-ABL1-negative hematopoiesis, CD26+ LSC engrafted NSG mice with BCR-ABL1+ cells. Functionally, CD26 was identified as target-enzyme disrupting the SDF-1alpha-CXCR4-axis by cleaving SDF-1alpha a chemotaxin for CXCR4+ stem cells. Whereas CD26 was found to inhibit SDF-1alpha-induced migration, CD26-targeting gliptins reverted this effect and blocked the mobilization of CML LSC in a stroma co-culture assay. CONCLUSIONS: CD26 is a robust biomarker of LSC and a useful tool for their quantification and isolation in patients with BCR/ABL1+ CML. Moreover, CD26 expression may explain the extramedullary spread of LSC in CML.
2014-04-17 | GSE40721 | GEO
Project description:BACKGROUND: BCR-ABL1+ chronic myeloid leukemia (CML) is characterized by abnormal production of leukemic stem (LSC) and progenitor cells and their spread from the bone marrow into the blood resulting in extramedullary myeloproliferation. So far, little is known about specific markers and functions of LSC in CML. METHODS: We examined the phenotype and function of CD34+/CD38─/Lin─ CML LSC by a multi-parameter screen approach employing antibody-phenotyping, mRNA expression profiling, and functional studies, including LSC repopulation experiments in irradiated NOD-SCID-IL-2Rgamma-/- (NSG) mice, followed by marker-validation using diverse control-cohorts and follow-up samples of CML patients treated with imatinib. RESULTS: Of all LSC markers examined, dipeptidylpeptidase IV (DPPIV=CD26) was identified as specific and functionally relevant surface marker-enzyme on CD34+/CD38─ CML LSC. CD26 was not detected on normal CD34+/CD38─ stem cells or LSC in other hematopoietic malignancies. The percentage of CD26+ CML LSC decreased to undetectable levels during successful treatment with imatinib in all patients (p<0.001). Whereas the sorted CD26─ stem cells obtained from CML patients engrafted irradiated NSG mice with multilineage BCR-ABL1-negative hematopoiesis, CD26+ LSC engrafted NSG mice with BCR-ABL1+ cells. Functionally, CD26 was identified as target-enzyme disrupting the SDF-1alpha-CXCR4-axis by cleaving SDF-1alpha a chemotaxin for CXCR4+ stem cells. Whereas CD26 was found to inhibit SDF-1alpha-induced migration, CD26-targeting gliptins reverted this effect and blocked the mobilization of CML LSC in a stroma co-culture assay. CONCLUSIONS: CD26 is a robust biomarker of LSC and a useful tool for their quantification and isolation in patients with BCR/ABL1+ CML. Moreover, CD26 expression may explain the extramedullary spread of LSC in CML. To define specific mRNA expression patterns and to identify specific LSC markers in CML LSC, gene array analyses were performed. RNA was isolated from sorted CD34+/CD45+/CD38─ CML LSC, CD34+/CD45+/CD38+ CML progenitor cells, CML MNC, sorted CD34+/CD38─ cord blood (CB) SC, CB-derived CD34+/CD38+ progenitor cells, and CB MNC. Total RNA was extracted from sorted cells using RNeasy Micro-Kit (Qiagen) and used (100 ng total RNA) for Gene Chip analyses. Preparation of terminal-labeled cRNA, hybridization to genome-wide human PrimeView GeneChips (Affymetrix, Santa Clara, CA, USA) and scanning of arrays were carried out according to the manufacturer's protocols (https://www.affymetrix.com). Robust Multichip Average (RMA) signal extraction and normalization were performed according to http://www.bioconductor.org/ as described.18 Differences in mRNA expression levels (from multiple paired samples) were calculated as mRNA ratio of i) CML LSC versus CB SC, ii) CML LSC versus CD34+/CD38+ CML progenitors, and normal cord blood SC versus cord blood progenitors. To calculate differential gene expression between individual sample groups where appropriate, we performed a statistical comparison using the LIMMA package as described previously. Briefly, LIMMA estimates the fold change between predefined sample groups by fitting a linear model and using an empirical Bayes method to moderate the standard errors of the estimated log-fold changes for each probe set.
2014-04-17 | E-GEOD-40721 | biostudies-arrayexpress
Project description:Monocytic leukemia cell line, THP-1 cells are known to respond to CXCL14. To identfy transcriptional regulation of CXCL14 signalling, we analyse gene expression changed with CXCL14 treatment. THP-1 treated with CXCL14 or PBS treated sample were used.
2013-12-17 | E-GEOD-44550 | biostudies-arrayexpress
Project description:Monocytic leukemia cell line, THP-1 cells are known to respond to CXCL14. To identfy transcriptional regulation of CXCL14 signalling, we analyse gene expression changed with CXCL14 treatment.
2013-12-17 | GSE44550 | GEO
Project description:Cxcl14+/- mice were mated with Cxcl14+/- mice, the embryos of pregnant females were collected on E13.5. After genotyping, the maternal part and fetal part of Cxcl14-/- and Cxcl14+/+ placentas were dissect out to extract total RNA respectively (n = 3). Total RNA was extracted using PureYield™ RNA Midiprep System (Promega).The maternal part of placenta that contained mesometrial lymphoid aggregate of pregnancy (MLAp) and decidua basalis (DB); the fetal part ofplacenta consisted of spongiotrophoblast and labyrinthin layer.Microarray hybridization was performed using a Mouse NimbleGen cDNA Microarray Kit (Roche), at CapitalBio Co., Ltd.(Beijing,China). Primary data were scaned using NimbleGen MS200 (Roche), and then extracted using NimbleScan system (Roche). Cxcl14+/- mice were mated with Cxcl14+/- mice, the embryos of pregnant females were collected on E13.5. After genotyping, the maternal part and fetal part of Cxcl14-/- and Cxcl14+/+ placentas were dissect out to extract total RNA respectively (n = 3). Total RNA was extracted using PureYield™ RNA Midiprep System (Promega).The maternal part of placenta that contained mesometrial lymphoid aggregate of pregnancy (MLAp) and decidua basalis (DB); the fetal part ofplacenta consisted of spongiotrophoblast and labyrinthin layer.Microarray hybridization was performed using a Mouse NimbleGen cDNA Microarray Kit (Roche), at CapitalBio Co., Ltd.(Beijing,China). Primary data were scaned using NimbleGen MS200 (Roche), and then extracted using NimbleScan system (Roche).
2013-06-19 | E-GEOD-48095 | biostudies-arrayexpress
Project description:In an attempt to identify novel markers and immunologic targets in leukemic stem cells (LSC) in acute myeloid leukemia (AML) and chronic myeloid leukemia (CML), we screened samples of patients with AML, CML, and controls for expression of cell surface antigens on CD34+/CD38− and CD34+/CD38+ cells by multi-color flow cytometry. In addition, we examined mRNA expression profiles in highly purified CD34+/CD38− and CD34+/CD38+ cells by gene array- and qPCR analyses. Aberrantly expressed markers were identified in all patient cohorts examined.
2020-09-21 | GSE138883 | GEO
Project description:Cxcl14+/- mice were mated with Cxcl14+/- mice, the embryos of pregnant females were collected on E13.5. After genotyping, the maternal part and fetal part of Cxcl14-/- and Cxcl14+/+ placentas were dissect out to extract total RNA respectively (n = 3). Total RNA was extracted using PureYield™ RNA Midiprep System (Promega).The maternal part of placenta that contained mesometrial lymphoid aggregate of pregnancy (MLAp) and decidua basalis (DB); the fetal part ofplacenta consisted of spongiotrophoblast and labyrinthin layer.Microarray hybridization was performed using a Mouse NimbleGen cDNA Microarray Kit (Roche), at CapitalBio Co., Ltd.(Beijing,China). Primary data were scaned using NimbleGen MS200 (Roche), and then extracted using NimbleScan system (Roche).
2013-06-19 | GSE48095 | GEO
Project description:Epithelial ovarian cancer (EOC) constitutes a major gynecological malignancy, with a reported incidence rate of 3-12/100 000 woman annually. As early symptoms of ovarian cancer are often clinically atypical or absent, the majority of ovarian cancer patients are diagnosed at a late stage, when the five-year survival rate is extremely low. This condition underscores the urgency of early detection of these patients and establishment of new therapeutic targets for successful intervention. Considering that the predominant biological characteristic that differentiates malignant from benign tumors is the ability to metastasize, it is necessary to identify novel metastasis-related molecules for ovarian cancer. In this study, we found that CAFs could significantly increase the metastatic potential of ovarian cancer cells compared with non-cancer associated fibroblasts(NAFs), which is associated with over-expression of CXCL14 in CAFs. We examined the impact of CAF-secreted CXCL14 on the lncRNA expression profiles in ovarian cancer during metastasis. We treated A2780s ovarian cancer cell line with recombinant CXCL14 protein and control respectively and subjected them to Arraystar Human LncRNA microarray v3.0 to profile differential lncRNAs in ovarian cancer upon treatment of CXCL14
2016-06-01 | E-GEOD-82059 | biostudies-arrayexpress
Project description:CXCL14, a recently described chemokine constitutively expressed in various epithelia, has multiple putative roles in inflammation and carcinogenesis. Based on the knowledge that cigarette smoking and the smoking-induced disorders, such as chronic obstructive pulmonary disease (COPD) and lung cancer, are associated with inflammation, we hypothesized that the airway epithelium, the primary site of smoking-induced pathologic changes in COPD and adenocarcinoma, responds to cigarette smoking with an altered CXCL14 gene expression as a part of disease-relevant molecular phenotype. Microarray analysis with subsequent TaqMan PCR validation revealed very low constitutive CXCL14 gene expression in the airway epithelium of healthy nonsmokers (n=53) which was strongly up-regulated in healthy smokers ( n=59; p<0.001) and further increased in COPD smokers (n=23; p<10-7 vs nonsmokers; p<0.005 vs healthy smokers). In smokers, CXCL14 expression inversely correlated with lung function parameters FEV1 and FEV1/FVC. Genome-wide analysis also showed that up-regulated correlation of CXCL14 expression with genes related to cell growth and proliferation, squamous differentiation and cancer. The analysis of 193 lung adenocarcinoma samples demonstrated a dramatic up-regulation of CXCL14 in a smoking-dependent manner. [need to include survival data once we get it]. Together, these data suggest that smoking-induced expression of CXCL14 in association with genome-wide reprogramming of processes related to tissue homeostasis, differentiation and tumorigenesis, represents a novel molecular link between cigarette smoking, COPD and lung cancer.
2024-06-05 | GSE21359 | GEO