Similar Datasets
Project description:Bulk RNA-seq profiling of CT26-bearing BALB/c mice across spleen, tumor, and tumor draining lymph node under multiple treatment regimens (Isotype, PD1, CYTO, PD1/CYTO, TS/CYTO, TS/PD1/CYTO) at study days 16 and 23.
2026-08-04 | GSE342349 | GEO
Project description:T cell infiltration is essential for immune checkpoint inhibitors to be effective in treating solid cancers. Through a bioinformatic pipeline, we identified a target gene SUN1 that might relate to modulating immune cell infiltration and immune response. Thus, we generated one Sun1_knockout CT26 cell line (Sun1_KO) and two control CT26 cell lines (Sun1_Control) using CRISPR-Cas9. By performing RNA-seq on cultured cells, tumors grown in syngeneic model, and purified tumor cells from tumors grown in syngeneic model, we set out to understand how mouse Sun1 can affect immune-related pathways and immune cell infiltration and anti-PD1 efficacy in BALB/c mice.
2024-03-29 | GSE250602 | GEO
Project description:Although membrane-anchored Pd-l1 has been well-studied for its engagement with PD-1 on T cells to evade anti-tumor immunity, whether Pd-l1 regulate oncogenic signaling pathways in tumor cells remains elusive. In this experiment, to further dissect roles of the K262 residue acetylation for Pd-l1 nuclear function, we profiled RNA expression of WT or K262Q mutant mouse Pd-l1 re-expressed in CT26 KO Pd-l1 cells. Methods: Total RNA fromCT26/Vector, CT26/WT or CT26 Pd-l1 KO cells was purified using Qiagen RNeasy mini kit (Qiagen) according to the manufacturer’s instructions. Library preparation and sequenceing analysis were performed by BGI-Hong Kong Co. Ltd. Conclusions: Our study indicates that Pd-l1 acetylation modification may affect its function in nuclear.
2020-06-07 | GSE146557 | GEO
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 CT26 cell lines and TGF-M-NM-21 knock-down CT26 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 CT26 cell lines and controls.Three-condition experiment: Locked nucleic acid microarray analyses to obtain miRNA expression profiles independently in TGFM-NM-21-knocked down CT26 and control cell line at three different time (24hours, 48hours and 72hours).Biological replicates: 1 CT26 cells stably transfected with shRNA-TGF-M-NM-21- pSUPER gfp-neo for 24hours, 1 CT26 cells stably transfected with shRNA-TGF-M-NM-21- pSUPER gfp-neo for 48hours, 1 CT26 cells stably transfected with shRNA-TGF-M-NM-21- pSUPER gfp-neo for 72hours, 1 CT26 cells stably transfected with shRNA-Control- pSUPER gfp-neo for 24hours, 1 CT26 cells stably transfected with shRNA- Control- pSUPER gfp-neo for 48hours, 1 CT26 cells stably transfected with shRNA-Control- pSUPER gfp-neo for 72hours, independently grown and harvested. One replicate per array.
2013-12-16 | E-GEOD-53337 | biostudies-arrayexpress
Project description:We have explored at the genome-wide expression level the effects of the novel HDAC inhibitor CXD101. In human CRC cell lines, a diverse set of differentially expressed genes were up- and down-regulated. Functional profiling of the expression data highlighted immune-relevant concepts related to antigen processing and natural killer (NK) cell mediated cytotoxicity. Similar gene profiles were apparent when global gene expression was investigated in murine CT26 cells treated with CXD101, which were also apparent in syngeneic CT26 tumours growing in vivo. The ability of CXD101 to affect immune-relevant gene expression coincided with changes in the tumour micro-environment (TME), especially in the sub-groups of tumour-infiltrating lymphocytes which occurred upon CXD101 treatment. The altered TME reflected synergistic anti-tumour activity apparent when CXD101 was combined with immune oncology (IO) agents, like anti-PD1 and anti-CTLA4.The ability of CXD101 to instate antigen presentation and augment NK activity in the TME, combined with the synergy between HDAC inhibitors and IO agents, provides a powerful rationale for exploring the combination effect in human cancers.
2021-06-30 | GSE158164 | GEO
Project description:Functional impairment of the immune response to chronic viral infections and malignancies is characterised by exhausted T cells, which do not respond to antigen. The cell surface receptor PD1 has been implicated in the maintenance of T cell exhaustion and is an attractive target for immunomodulatory approaches to the treatment of such conditions. However, the mechanisms by which PD1 signalling causes exhaustion and the exact response of T cells to PD1 activation are not clear although it has been suggested that PD1 up regulates a number of anti-proliferative factors. Here we perform cytokine and transcriptional profiling of uninfected primary human T cells to characterise these events. We find that PD1 completely prevents cytokine and transcrip- tional changes induced by CD3/28 stimulation. We do not see any factors specifically induced by PD1, including BATF or IL10 which have previously been linked to PD1 activity. Together with the work of others this confirms that PD1 is the sole effector of T cell exhaustion and that infection is responsible for BATF and IL10 up regulation. As a consequence future therapeutic strategies will be confined to the inhibition of PD1 and not a downstream effector.
2012-04-01 | E-MEXP-3410 | biostudies-arrayexpress
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 CT26 cell lines and TGF-β1 knock-down CT26 cell lines. We identified a novel set of TGF-β1-related miRNAs.
2013-12-16 | GSE53337 | GEO