Ontology highlight
ABSTRACT:
PROVIDER: PRJNA798081 | ENA |
REPOSITORIES: ENA
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Project description:We used a streamlined pipeline for the generation of personalized cancer vaccines starting from the isolation and selection of the most immunogenic peptide candidates expressed on the tumour cells and ending in the generation of efficient therapeutic oncolytic cancer vaccines. We used MHC-I immunoaffinity purification in a murine colon tumor model from CT26 cells. The selection of the target candidates was then based on two separate approaches: RNAseq analysis and HEX software.
2022-04-06 | PXD026463 | Pride
Project description:A number of studies have reported evidence of positive or negative contributions of galectin-9 (gal-9) to human and experimental malignancies. Some clinical observations and in vitro experiments suggest that cell-associated gal-9 has anti-metastatic effects. On the other hand, extra-cellular gal-9 consistently enhances tumor immune escape. The aim of this experiment is to study the impact of gal-9 gene invalidation in the colon carcinoma cell line CT26, in vitro. It complements the results of a RNAseq analysis carried out using the same cells, whose results are already available on Annotare (E-MTAB-9559)
2021-01-01 | E-MTAB-9837 | biostudies-arrayexpress
Project description:First, lentivirus-mediated overexpression of FDFT1 and lentivirus-mediated knockdown of FDFT1 were performed in CT26 cells. Then control CT26 cells, FDFT1 overexpressing CT26 cells and FDFT1 knockdown CT26 cells were cultured under normal medium or fasting mimic medium. Fasting mimic medium was done by incubating cells in glucose-free DMEM (Gibco, USA) supplemented with 0.5g/L glucose and 1% FBS for 48h. So we have 6 groups: control CT26 cells, FDFT1 overexpressing CT26 cells, FDFT1 knockdown CT26 cells, control CT26 cells-under fasting mimic medium, FDFT1 overexpressing CT26 cells- under fasting mimic medium, FDFT1 knockdown CT26 cells- under fasting mimic medium.
2020-03-19 | PXD012029 | Pride
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:RNA sequencing data of CT26-shppp2r1a and CT26-scr samples
| PRJNA756949 | ENA
Project description:Selenium has cancer preventive activity that is mediated, in part, through selenoproteins. The role of the 15 kDa selenoprotein (Sep15) in colon cancer was assessed by preparing and using mouse colon CT26 cells stably transfected with shRNA constructs targeting Sep15. Metabolic 75Se-labeling and Northern and Western blot analyses revealed that more than 90% of Sep15 was knocked down. Growth of the resulting Sep15-deficient CT26 cells was reduced (p<0.01) and cells formed significantly (p<0.001) fewer colonies in soft agar compared to control CT26 cells. Whereas most (14/15) BALB/c mice injected with control cells developed tumors, few (3/30) mice injected with Sep15 knockdown cells developed tumors (p<0.0001). The ability to form pulmonary metastases had similar results. Mice injected with the plasmid-transfected control cells had >250 lung metastases/mouse; however, mice injected with the Sep15 knockdown cells only had 7.8 +/- 5.4 metastases. To investigate molecular targets affected by Sep15 status, gene expression patterns between control and knockdown CT26 cells were compared. Ingenuity Pathways Analysis was used to analyze the 1045 genes that were significantly (p<0.001) affected by Sep15 deficiency. The highest scored biological functions were cancer and cellular growth and proliferation. Consistent with these observations, subsequent analyses revealed a G2/M cell cycle arrest in Sep15 CT26 knockdown cells. In contrast, to CT26 cells Sep15 knockdown in Lewis Lung Carcinoma (LLC1) cells did not affect anchorage-dependent or M-bM-^@M-^Sindependent cell growth. These data suggest tissue specificity in the cancer protective effects of Sep15 knockdown, which are mediated, at least in part, by influencing the cell cycle. mRNA was isolated from plasmid-transfected control and shSep15 knockdown CT26 cells (three replicates of each). Microarray analysis was performed on Affymetrix Mouse 430_2 gene chips. Three arrays were analyzed from different mRNA samples for each construct.
2010-07-06 | E-GEOD-20390 | biostudies-arrayexpress
Project description:Selenium has cancer preventive activity that is mediated, in part, through selenoproteins. The role of the 15 kDa selenoprotein (Sep15) in colon cancer was assessed by preparing and using mouse colon CT26 cells stably transfected with shRNA constructs targeting Sep15. Metabolic 75Se-labeling and Northern and Western blot analyses revealed that more than 90% of Sep15 was knocked down. Growth of the resulting Sep15-deficient CT26 cells was reduced (p<0.01) and cells formed significantly (p<0.001) fewer colonies in soft agar compared to control CT26 cells. Whereas most (14/15) BALB/c mice injected with control cells developed tumors, few (3/30) mice injected with Sep15 knockdown cells developed tumors (p<0.0001). The ability to form pulmonary metastases had similar results. Mice injected with the plasmid-transfected control cells had >250 lung metastases/mouse; however, mice injected with the Sep15 knockdown cells only had 7.8 +/- 5.4 metastases. To investigate molecular targets affected by Sep15 status, gene expression patterns between control and knockdown CT26 cells were compared. Ingenuity Pathways Analysis was used to analyze the 1045 genes that were significantly (p<0.001) affected by Sep15 deficiency. The highest scored biological functions were cancer and cellular growth and proliferation. Consistent with these observations, subsequent analyses revealed a G2/M cell cycle arrest in Sep15 CT26 knockdown cells. In contrast, to CT26 cells Sep15 knockdown in Lewis Lung Carcinoma (LLC1) cells did not affect anchorage-dependent or –independent cell growth. These data suggest tissue specificity in the cancer protective effects of Sep15 knockdown, which are mediated, at least in part, by influencing the cell cycle.
2010-07-07 | GSE20390 | GEO
Project description:To systematically examine the effect of tumor cells on macrophages, the RAW264.7 cells after a 24-hour coculture with CT26 cells were subjected to RNA sequencing, the complete medium of CT26 cells were used as control.
2022-10-02 | GSE214450 | GEO
Project description:The goal was to identify genes that promote liver metastasis of colorectal cancer. Microarray analysis was performed to compare gene expression and altered biological pathways between a poorly metastatic CT26 cell line as compared to an isogenic highly metastatic CT26 FL3 cell line that was isolated by in vivo selection in an orthotopic mouse model of colon cancer metastasis to the liver. Gene expression in CT26-FL3 and parental CT26 cells were determined using the Agilent platform. Four independent samples each were analyzed.
2016-03-30 | E-GEOD-67675 | biostudies-arrayexpress
Project description:RNAseq on tumors isolated from CT26 tumor bearing mice
| PRJNA641847 | ENA