Similar Datasets
Project description:We examined the metastasis-related miRNAs induced by SDF-1/CXCR4 system, using oral cancer cells. Consequently, we identified 4 kinds of upregulated-miRNAs in B88-SDF-1.
2015-08-01 | GSE59323 | GEO
Project description:We examined the metastasis-related miRNAs induced by SDF-1/CXCR4 system, using oral cancer cells. Consequently, we identified 4 kinds of upregulated-miRNAs in B88-SDF-1. The metastasis-related miRNAs induced by SDF-1/CXCR4 system in oral cancer are largely unknown. Thus, we examined the metastasis-related miRNAs induced by SDF-1/CXCR4 system, using four types of oral cancer cells; mock cells vs forced-expression of SDF-1cells and parental cells vs parental cells treated by SDF-1.
2015-08-01 | E-GEOD-59323 | biostudies-arrayexpress
Project description:SDF-1 has been reported to trigger ADAMTS4,5 overexpression through activating CXCR4 signaling in chondrocytes. Here we described the transcriptional changes of SDF-1-treatment as well as natural products CXCR4 antagonists treatment.
2022-03-09 | GSE197921 | GEO
Project description:The changes in non-coding RNA i.e. microRNA profile in the response to stromal derived factor-1 treatment of the mouse satellite cell derived myoblasts. RNA was isolated from SC-derived myoblasts transfected with siRNA complementary to mRNA encoding CXCR4, CXCR7 (SDF-1 receptors) or treated with SDF-1.
2023-04-07 | E-MTAB-12810 | biostudies-arrayexpress
Project description:We triggered the involvement of lncRNAs in odontogenic differentiation of DPSCs by incubation with SDF-1α. By LncRNA microarray, alterations in lncRNA expression at odontogenic differentiation inducted by 100ng/Ml SDF-1α were identified. Quantitative reverse transcription polymerase chain reaction (qRT-PCR) was used to validate several random upregulated and downregulated LncRNAs in the odontogenic differentiation of DPSCs. In addition, Gene ontology (GO) analysis and coding-noncoding gene coexpression (CNC) analysis were conducted to predict the interactions of coding and noncoding RNA and identify core regulatory factors in odontogenic differentiation of DPSCs.
2021-09-02 | GSE183162 | GEO
Project description:We have employed whole genome microarray expression profiling to identify genes differentially expressed in cord blood enriched CD34+ cells(>95%) after a short-term exposure to the chemokine stromal cell-derived factor-1 (SDF-1). SDF-1 induced gene expressions of cord blood enriched CD34+ cells were measured at 4 hours. Four biological replicates were performed for each treatment group.
2011-01-01 | E-GEOD-20891 | biostudies-arrayexpress
Project description:We have employed whole genome microarray expression profiling to identify genes differentially expressed in cord blood enriched CD34+ cells(>95%) after a short-term exposure to the chemokine stromal cell-derived factor-1 (SDF-1).
2011-01-01 | GSE20891 | GEO
Project description:In colorectal cancer, increased expression of the CXC chemokine receptor 4 (CXCR4) has been shown to provoke metastatic disease due to the interaction with its ligand stromal cell-derived factor 1 (SDF-1). Recently, a second SDF-1 receptor, CXCR7, was found to enhance tumor growth in solid tumors. Albeit signaling cascades via SDF-1/CXCR4 have been intensively studied, the significance of the SDF-1/CXCR7-induced intracellular communication triggering malignancy is still only marginally understood. In tumor tissue of 52 colorectal cancer (CRC) patients, we observed that expression of CXCR7 and CXCR4 increased with tumor stage, tumor size, and lymph node infiltration. Asking whether activation of CXCR4 or CXCR7 might result in a similar expression pattern, we performed microarray expression analyses using lentivirally CXCR4- and/or CXCR7-overexpressing SW480 colon cancer cell lines with and without stimulation by SDF-1α. Gene regulation via SDF-1α/CXCR4 and SDF-1α/CXCR7 was completely different and partly antidromic. Expressions of the differentially expressed genes AKR1C3, AXL, EGFR, IGFBP7, IL24, TNNC1, TRIP6 were confirmed by qPCR. Differentially regulated genes were assigned by GO to migration and lipid metabolic processes. Furthermore, using the in silico gene set enrichment analysis we showed for the first time that expressions of miR-217 and miR-218 were increased in CXCR4 and reduced in CXCR7 cells after stimulation with SDF-1α. As expected, their putative target mRNAs were inversely expressed. Functional assays exerted that exposure to SDF-1α resulted in strongly amplified invasiveness and chemosensitivity of CXCR4-expressing cells. CXCR7 overexpression led to reduced invasiveness which could only be marginally increased by SDF-1α. The CXCR4 antagonist plerixafor significantly reduced invasiveness of CXCR4-overexpressing cells only. Similarly, compared to control cells, CXCR4 cells showed increased sensitivity against 5-FU, while CXCR7 cells were more chemoresistant. These opposing results for CXCR4- or CXCR7-overexpressing colon carcinoma cells demand an unexpected attention in the clinical application of chemokine receptor antagonists like Plerixafor.
2012-08-10 | GSE40017 | GEO
Project description:Robust genes were up-regulated in the oral cancer cells with SDF-1/CXCR4 system; however, most of the genes did not exhibit metastasis-related functions. Mock cells and B88-SDF-1 cells, which have an autocrine SDF-1/CXCR4 system and exhibit distant metastatic potential in vivo were used.
2013-12-31 | E-GEOD-50507 | biostudies-arrayexpress
Project description:In colorectal cancer, increased expression of the CXC chemokine receptor 4 (CXCR4) has been shown to provoke metastatic disease due to the interaction with its ligand stromal cell-derived factor 1 (SDF-1). Recently, a second SDF-1 receptor, CXCR7, was found to enhance tumor growth in solid tumors. Albeit signaling cascades via SDF-1/CXCR4 have been intensively studied, the significance of the SDF-1/CXCR7-induced intracellular communication triggering malignancy is still only marginally understood. In tumor tissue of 52 colorectal cancer (CRC) patients, we observed that expression of CXCR7 and CXCR4 increased with tumor stage, tumor size, and lymph node infiltration. Asking whether activation of CXCR4 or CXCR7 might result in a similar expression pattern, we performed microarray expression analyses using lentivirally CXCR4- and/or CXCR7-overexpressing SW480 colon cancer cell lines with and without stimulation by SDF-1M-NM-1. Gene regulation via SDF-1M-NM-1/CXCR4 and SDF-1M-NM-1/CXCR7 was completely different and partly antidromic. Expressions of the differentially expressed genes AKR1C3, AXL, EGFR, IGFBP7, IL24, TNNC1, TRIP6 were confirmed by qPCR. Differentially regulated genes were assigned by GO to migration and lipid metabolic processes. Furthermore, using the in silico gene set enrichment analysis we showed for the first time that expressions of miR-217 and miR-218 were increased in CXCR4 and reduced in CXCR7 cells after stimulation with SDF-1M-NM-1. As expected, their putative target mRNAs were inversely expressed. Functional assays exerted that exposure to SDF-1M-NM-1 resulted in strongly amplified invasiveness and chemosensitivity of CXCR4-expressing cells. CXCR7 overexpression led to reduced invasiveness which could only be marginally increased by SDF-1M-NM-1. The CXCR4 antagonist plerixafor significantly reduced invasiveness of CXCR4-overexpressing cells only. Similarly, compared to control cells, CXCR4 cells showed increased sensitivity against 5-FU, while CXCR7 cells were more chemoresistant. These opposing results for CXCR4- or CXCR7-overexpressing colon carcinoma cells demand an unexpected attention in the clinical application of chemokine receptor antagonists like Plerixafor. 24 samples
2012-08-09 | E-GEOD-40017 | biostudies-arrayexpress