Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR18737878_1.fastq.gz | Fastqsanger.gz | |||
| SRR18737878_2.fastq.gz | Fastqsanger.gz |
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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: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: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: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: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:Given that TREX1-deficient tumor cells showed a growth delay in immunocompetent but not immunodeficient hosts, we characterize the consequences of CT26 tumor-intrinsic TREX1 loss on the host immune system by performing single-cell RNA sequencing on intra-tumoral immune cells sorted from control and TREX1 KO CT26 tumors.
2024-03-12 | E-MTAB-13823 | biostudies-arrayexpress
Project description:Stable Isotope Labeling using Amino acids in Cell culture (SILAC) of CT26 control and IF1-ablated cells
2023-10-24 | PXD038109 | Pride