Murine Kras mutant or Kras wildtype cancer cell lines
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA540827 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Comparison of gene expression in murine Kras mutant (LLC, AE17, MC38, FULA1) and Kras wildtype cell lines (B16F10, PANO2, CULA). First gene expression of benign cells and tissue ( BMDM, TEC, LUNG, BMMC) was subtracted from both Kras mutant or Kras wildtype gene expression profiles. Second Kras mutant gene expression was compared to Kras wildtype gene expression. Cell lines expressing genetically modified Kras gene were included in the analysis. Genetic modification was either done by overexpression of mutant KRAS harboring a G12C mutation or silencing with shRNA targeting Kras. shControl cell lines were used also as wildtype samples in different analysis presented in the manuscript except MC38 ( run on chip MoGene_1.0).
2022-05-02 | GSE130624 | GEO
Project description:We investigated the transcriptomic effect of GNAS(R201C) expression in murine cell lines derived from the Kras;Gnas model of pancreatic intraductal papillary mucinous neoplasms where transgenic mutant GNAS is doxycycline inducible (LGKC; p48(Cre), Kras(LSL-G12D), Rosa26(LSL-rtTA)), Tg(TetO-GNAS(R201C)) using bulk RNA-seq.
2024-09-15 | GSE275403 | GEO
Project description:KRAS inhibitors such as Sotorasib and Adagrasib are reshaping the treatment landscape for G12C mutant cancers, yet durable responses remain limited by the emergence of drug tolerant persister (DTP) cells that survive initial therapy and drive relapse. Here, we identify a metabolic program centered on α ketoglutarate (α KG) that enables KRAS G12C–mutant pancreatic and lung cancer cells to withstand inhibitor pressure.
2026-04-22 | PXD067380 | JPOST Repository
Project description:The experiment is a study of the effects of signal strength in the Ras pathway. In particular, we studied a gain-of-function mutant of Kras, KrasG12D. We generated these mutant mice and performed microarray analyses on RNA extracted from whole skin, comparing KrasG12D mice to wild-type mice, with three replicates of each.
2011-06-03 | E-MTAB-700 | biostudies-arrayexpress
Project description:KRAS is mutated in over 90% of pancreatic ductal adenocarcinomas (PDAC), where hotspot alterations in codons 12, 13, and 61 drive tumor initiation and progression. Although distinct biochemical properties have been described for individual KRAS mutants, whether they generate unique allele-specific signaling programs in PDAC cells remains unresolved. Here, we systematically interrogated the molecular consequences of seven common KRAS mutant variants by reconstituting isogenic, KRAS-deficient PDAC cell lines and performing integrated transcriptomic, proteomic, and phosphoproteomic profiling.
2026-09-10 | PXD071086 | Pride
Project description:KRAS mutant cancers, which feature the activation of multiple phosphorylation signaling pathways, remain a major challenge for cancer therapy. This study provides a landscape of the proteomics and phosphoproteomics of KRAS mutant cancers by analyzing different KRAS mutant human cancer cell lines across different tissues types. By integrating multi-omics analysis, we identify different robust subsets, which recapitulate the histological, pathological and prognostic features of human cancers.
2021-06-23 | PXD026892 |
Project description:KRas is one of the most prevalent mutations in pancreatic cancer and derives diverse signalling cascades to support tumour initiation and progression. Pancreatic ductal adenocarcinoma (PDAC) is the most diagnosed type of pancreatic cancer and is characterized to have a very dense stromal rigidity. Therapeutic targeting of KRas mutant tumours is hard to achieve due to a deficit in the direct targeting of KRas and the existence of multiple compensatory pathways downstream of mutant KRas. Thus, we used a proximity labelling technique (BioID) coupled with mass spectrometry to identify the interactors for mutant KRas (G12D mutation) in PDAC organoid models of murine origin. Bioinformatics analysis revealed a network of 95 proteins in the proximity of mutant KRas including canonical interactors, ECM molecules, integrins and RTKs.
2026-09-11 | PXD069991 | Pride
Project description:RNA sequencing of wildtype-KRAS HKE3 (wtHKE3) and mutant-KRAS HKE3 (mtHKE3) colorectal cancer cell lines before and after stimulation with TGF-alpha
| PRJNA434191 | ENA
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
Project description:KRas is one of the most prevalent mutations in pancreatic cancer and derives diverse signalling cascades to support tumour initiation and progression. Pancreatic ductal adenocarcinoma (PDAC) is the most diagnosed type of pancreatic cancer and is characterized to have a very dense stromal rigidity. Therapeutic targeting of KRas mutant tumours is hard to achieve due to a deficit in the direct targeting of KRas and the existence of multiple compensatory pathways downstream of mutant KRas. Thus, we used a proximity labelling technique (BioID) coupled with mass spectrometry to identify the interactors for mutant KRas (G12V mutation) in pancreatic cancer cell lines and a normal pancreatic ductal epithelial cell line. Bioinformatics analysis revealed a network of 126 proteins in the proximity of mutant KRas including canonical interactors, ECM molecules, integrins and RTKs. Further experimentation revealed extensive crosstalk between RTKs-mediated aberrant KRas signalling and integrins signalling to support PDAC survival and progression. Thus, this study highlighted the convergence of three major signalling pathways in pancreatic cancer which may explain their role in deriving the stromal rigidity and failure of therapeutic targeting of KRas mutant cancers.
2026-09-11 | PXD069779 | Pride