Project description:The goal of the current study was to identify miRNAs regulated by TGF-b in human CD8+ T cells and analyze the function of these miRNAs in shaping the immunomodulatory effect of TGF-b in these cells. We identified the miR-23a cluster to be upregulated and found that this cluster could target key molecules (IFN-g and LAMP1) involved in immune response by CD8+ T cells.
Project description:The goal of the current study was to identify miRNAs regulated by TGF-b in human CD8+ T cells and analyze the function of these miRNAs in shaping the immunomodulatory effect of TGF-b in these cells. We identified the miR-23a cluster to be upregulated and found that this cluster could target key molecules (IFN-g and LAMP1) involved in immune response by CD8+ T cells.
Project description:The goal of the current study was to identify miRNAs regulated by TGF-b in human CD8+ T cells and analyze the function of these miRNAs in shaping the immunomodulatory effect of TGF-b in these cells. We identified the miR-23a cluster to be upregulated and found that this cluster could target key molecules (IFN-g and LAMP1) involved in immune response by CD8+ T cells. CD8+ T cells were isolated and purified from healthy human peripheral blood of 5 donors and were activated using beads coupled to anti-CD2, anti-CD3 and anti-CD24. They were then treated with 5ng/ml TGF-b, with 1µM SD-208 or left untreated. RNA from these cells were then isolated and used for deep sequencing.
Project description:The goal of the current study was to identify miRNAs regulated by TGF-b in human CD8+ T cells and analyze the function of these miRNAs in shaping the immunomodulatory effect of TGF-b in these cells. We identified the miR-23a cluster to be upregulated and found that this cluster could target key molecules (IFN-g and LAMP1) involved in immune response by CD8+ T cells. CD8+ T cells were isolated and purified from healthy human peripheral blood of 5 donors and were activated using beads coupled to anti-CD2, anti-CD3 and anti-CD24. They were then treated with 5ng/ml TGF-b, with 1M-BM-5M SD-208 or left untreated. RNA from these cells were then isolated and used for generating miRNA microarrays.
Project description:To investigate the role of TGF-β1-regulated miRNAs in the progression of colorectal cancer,we performed comprehensive miRMA microarray analysis on RNA derived from typical human colorectal cancer cell lines and TGF-β1 knock-down human colorectal cancer cell lines. We identified a novel set of TGF-β1-related miRNAs.
Project description:A miRNA microarray was used to identify candidate miRNAs regulated by PTHrP treatment in chondrogenic hMSC differentiation. miRNA-expression patterns after PTHrP treatment for 1 week (CM-T-Pt-L1) or 3 weeks (CM-T-Pt-3) in chondrogenic culture were compared with reference levels obtained from cell pellets treated with TGF-β only (CM-T). Under identical chondrogenesis conditions (except for PTHrP treatment), miRNA-expression patterns were relatively unchanged when compared with the TGF-β-only control, which simplified the selection of candidate miRNAs. Microarray analysis revealed that only 4 miRNAs in CM-T-Pt-L1 cells and 7 miRNAs in CM-T-Pt-3 cells were differentially expressed following PTHrP treatment. Hsa-miR-590-5p and hsa-miR-892b were commonly down-regulated or up-regulated in both PTHrP-treated groups. Interestingly, hsa-miR-892b expression was not detected in the TGF-β-only control, while hsa-miR-877*, hsa-miR-1288, and hsa-miR-1305 were up-regulated. Therefore, PTHrP treatment induced hsa-miR-892b expression during TGF-β-mediated hMSC chondrogenesis. hsa-miR-892b expression in CM-T-Pt-L1 cells was 2.43-fold higher than that in CM-T-Pt-3 cells.
Project description:To investigate the role of TGF-M-NM-21-regulated miRNAs in the progression of colorectal cancer,we performed comprehensive miRMA microarray analysis on RNA derived from typical human colorectal cancer cell lines and TGF-M-NM-21 knock-down human colorectal cancer cell lines. We identified a novel set of TGF-M-NM-21-related miRNAs. Total RNA was isolated from TGF-M-NM-21-knock down colorecatl cancer cell lines and controls.Three-condition experiment: shRNA-TGF-M-NM-21/Lovo cells vs. shRNA-Control/Lovo cells, shRNA-TGF-M-NM-21/SW620 cells vs. shRNA-Control/ SW620 cells, and shRNA-TGF-M-NM-21/HT29 cells vs. shRNA-Control/HT29 cells. Biological replicates: 1 Lovo cells stably transfected with shRNA-TGF-M-NM-21- pSUPER gfp-neo, 1SW620 cells stably transfected with shRNA-TGF-M-NM-21- pSUPER gfp-neo, 1HT29 cells stably transfected with shRNA-TGF-M-NM-21- pSUPER gfp-neo, 1Love cells stably transfected with shRNA-Control- pSUPER gfp-neo, 1SW620 cells stably transfected with shRNA-Control- pSUPER gfp-neo, and 1HT29 cells stably transfected with shRNA-Control- pSUPER gfp-neo, independently grown and harvested. One replicate per array.
Project description:To investigate the role of TGF-β1-regulated miRNAs in the progression of RMS,we performed comprehensive miRMA microarray analysis on RNA derived from typical RMS cell lines and TGF-β1 knock-down cell lines. We identified a novel set of TGF-β1-related miRNAs.