E-MTAB-9207
Ontology highlight
ABSTRACT:
PROVIDER: E-MTAB-9207 | ExpressionAtlas | 2025-01-16
REPOSITORIES: ExpressionAtlas
Similar Datasets
Project description:RNA-seq of HCT116 KRAS G13D and HCT116 KRAS WT cell lines with control or CFIm25 knockdown
| PRJEB38811 | ENA
Project description:HCT116 Kras WT and Kras G13D isogenic pair cell lines were cultured in either 25 mM or 1 mM for one week.
2012-07-01 | GSE31084 | GEO
Project description:HCT116 Kras WT and Kras G13D isogenic pair cell lines were cultured in either 25 mM or 1 mM for one week. Two independent replicate samples for each cell line and for each treatment were profiled using Affymetrix HG U133 plus 2.0 arrays
2012-06-30 | E-GEOD-31084 | biostudies-arrayexpress
Project description:Despite the advent of mutant-selective KRAS inhibitors, colorectal cancer (CRC) responses remain limited, with frequent stable disease and rapid recurrence. The mechanisms underlying CRC tolerance to KRAS inhibition and eventual resistance are poorly understood. Here, we explored early transcriptional and proteomic changes following KRAS silencing in 3D CRC spheroid models to identify pathways linked to sensitivity or resistance. Based on growth, cell cycle, and apoptosis responses, cell lines were classified as KRAS silencing-sensitive (HCT116, SW480) or -resistant (LS174T, SW837). Sensitive cells showed upregulation of the unfolded protein response (UPR) and WNT/β-catenin signaling, while these pathways were downregulated in resistant cells. Proteomic analysis confirmed UPR deregulation, with reduced translation-related proteins in sensitive cells. Functional assays revealed that KRAS knockdown in HCT116 reduced protein aggregation and translational capacity, consistent with UPR activation. However, inhibiting IRE1α-mediated UPR signaling did not reverse KRAS silencing-induced arrest or apoptosis. These findings suggest UPR activation as an early adaptive response in KRAS-dependent CRC cells.
2025-05-07 | PXD059013 | Pride
Project description:Raw data from E-MTAB-1585 was normalized by using reads per million. https://www.ebi.ac.uk/arrayexpress/experiments/E-MTAB-1585/ Strand specific RNA-Seq data E-MTAB-1585 was normalized and subtracted control from knockdown to generate tracks that more clearly displayed the unusual pattern of RNA expression caused by knockdown of 7SK. The following wig files were generated from multiple samples (i.e.raw data files), as indicated in the 'readme.txt' file. 7sk_3p_KD_norm.wig: 7SK 3P Knockdown normalized 7sk_3p_KDF_norm.wig: 7SK 3P Knockdown normalized (Forward) 7sk_3p_KDR_norm.wig: 7SK 3P Knockdown normalized (Reverse) 7sk_5p_KD_norm.wig: 7SK 5P Knockdown normalized 7sk_5p_KDF_norm.wig: 7SK 5P Knockdown normalized (Forward) 7sk_5p_KDR_norm.wig: 7SK 5P Knockdown normalized (Reverse) 7sk_Control_norm.wig: 7SK Control normalized 7sk_ControlF_norm.wig: 7SK Control normalized (Forward) 7sk_ControlR_norm.wig: 7SK Control normalized (Reverse) 7sk_3p_KDF-ControlF.wig: 7SK 3P Knockdown-Control (Forward) 7sk_3p_KDR-ControlR.wig: 7SK 3P Knockdown-Control (Reverse) 7sk_5p_KDF-ControlF.wig: 7SK 5P Knockdown-Control (Forward) 7sk_5p_KDR-ControlR.wig: 7SK 5P Knockdown-Control (Reverse)
2013-09-19 | E-GEOD-50860 | biostudies-arrayexpress
Project description:Recent studies have shown that circular RNAs (circRNAs) are abundant, widely expressed in mammals, and can display cell-type specific expression. However, how production of circRNAs is regulated and their precise biological function remains largely unknown. To study how circRNAs might be regulated during colorectal cancer progression, we used three isogenic colon cancer cell lines that differ only in KRAS mutation status. Cellular RNAs from the parental DLD-1 cells that contain both wild-type and G13D mutant KRAS alleles and isogenically-matched derivative cell lines, DKO-1 (mutant KRAS allele only) and DKs-8 (wild-type KRAS allele only) were analyzed using RNA-Seq. We developed a bioinformatics pipeline to identify and evaluate circRNA candidates from RNA-Seq data. Hundreds of high-quality circRNA candidates were identified in each cell line. Remarkably, circRNAs were significantly down-regulated at a global level in DLD-1 and DKO-1 cells compared to DKs-8 cells, indicating a widespread effect of mutant KRAS on circRNA abundance. This finding was confirmed in two independent colon cancer cell lines HCT116 (KRAS mutant) and HKe3 (KRAS WT). In all three cell lines, circRNAs were also found in secreted extracellular-vesicles, and circRNAs were more abundant in exosomes than cells. Our results suggest that circRNAs may serve as promising cancer biomarkers.
2017-10-01 | GSE72577 | GEO
Project description:To investigate the biological function TRIM21 in the colorectal cancer, we established HCT116 cell lines in which the TRIM21 gene has been knocked down by shRNA. We used a lentiviral shRNA technique to knockdown TRIM21 expression in HCT116 cells. A scrambled shRNA (shRNA/Control) was used as a control. We then performed RNA-Seq with Cloud-seq Biotech Inc. (Shanghai, China) to analyze gene expression changes in HCT116 cells. For each sample, three independent biological replicates were performed.
2023-05-23 | GSE211267 | GEO
Project description:The study aimed to identify genes essential for the maintenance of the transformed phenotype of the colorectal cancer cell line HCT116, which is dependent on the continued expression of the activated KRAS oncogene (KRASG13D). We generated HCT116 cell lines stably expressing an inducible shRNA-expressing retroviral vector targeting KRAS (Ngo et al., Nature, 2006). In cells engineered to express the bacterial tetracycline repressor, the shRNA is expressed specifically upon doxycycline addition. With this system, we showed that inducible down-regulation of KRAS is triggering cell death in the HCT116 cells, suggesting oncogene addiction in this cell line. In this study, we compared the gene expression profile of HCT116 cells where KRAS has been downregulated for different lengths of time, aiming at identifying RAS-target genes. We also compared the gene expression profile of the parental HCT116 cell line with two derived isogenic cell lines, Hke3 and Hkh-2, where the activated KRAS gene has been deleted by homologous recombination.
2022-04-03 | GSE199871 | GEO
Project description:KRAS signaling has been extensively studied, yet the clarification between KRAS-autonomous and non-autonomous mechanisms are still less explored. Understanding how KRAS signaling and effects are affected by exogenous stimuli can provide valuable insights not only to understand resistance mechanisms that justify pathway inhibition failure, but also to uncover novel therapeutic targets for mutant KRAS patients. Hence, aiming at understanding KRAS-autonomous versus non autonomous mechanisms, we studied the response of two mutant KRAS colorectal cancer cell lines (HCT116 and LS174T) - control and KRAS silenced- to TGFβ1-activated fibroblasts secretome. By performing a total proteome analysis, we observed that TGFβ1-activated fibroblast-secreted factors triggered cell-line specific proteome alterations and that mutant KRAS governs approximately 1/3 of those alterations. Moreover, the analysis of the impact of exogenous factors on the modulation of KRAS proteome revealed that more than 2/3 of the KRAS-associated proteome is controlled in a KRAS-non-autonomous manner, dependent on the exogeneous factors, in both cell lines. This work highlights the context-dependency of KRAS-associated signaling and reinforces the importance of establishing more integrative models resembling the complexity of the tumor microenvironment to study KRAS-associated signals.
2022-04-06 | PXD030551 | Pride