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MetabolomicsTargeting GSTZ1 sensitizes KRASG12C-mutant lung cancer cells by overcoming glutathione and glycolysis pathway rewiring

KRAS mutations are prevalent in lung cancer, but KRAS G12C inhibitors exhibit limited efficacy, partly due to metabolic adaptations, such as enhanced glutathione metabolism and increased glycolysis. Glutathione S-Transferase Zeta 1 (GSTZ1) is a metabolic enzyme that regulates cell metabolism. How...

2026-05-15 | MTBLS12791 | MetaboLights
MetabolomicsMetabolic profiling of induced acute pancreatitis and pancreatic cancer progression in a mutant Kras mouse model
Not available
ORGANISM(S): Mus musculus 
ST002202 | MetabolomicsWorkbench
ProteomicsA Systems Mechanism for KRAS Mutant Allele Specific Responses to Targeted Therapy
Cancer treatment decisions are increasingly guided by which specific genes are mutated within each patient’s tumor. For example, agents inhibiting the epidermal growth factor receptor (EGFR) benefit many colorectal cancer (CRC) patients, with the general exception of those whose tumor includes a KR...
ORGANISM(S): Homo sapiens (Human) 
2020-05-27 | PXD014755 | Pride
Thus resolving a problem in cancer personalized medicine. Systems approaches reveal why cancer patients with one specific kras mutation respond to egfr inhibitors 
ProteomicsTargeting ubiquitin-independent proteasome with small molecule increases susceptibility in pan-KRAS mutant cancers
Despite advances in the development of direct KRAS inhibitors, KRAS-mutant cancers continue to exhibit resistance to the currently available therapies. Here, we identified REGγ as a mutant KRAS-associated factor that enhances REGγ transcription through the KRAS intermediate NRF2, suggesting that the...
ORGANISM(S): Homo Sapiens 
2025-01-01 | PXD059364 |
ProteomicsA proteomic and phosphoproteomic landscape of KRAS mutant cancers identifies combination therapies
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 acr...
ORGANISM(S): Homo Sapiens 
2021-06-23 | PXD026892 |
TranscriptomicsKRAS-Dependent Sorting of miRNAs and other small RNAs to secreted vesicles
Although long thought to act cell autonomously, mutant KRAS colorectal cancer (CRC) cells release protein-laden exosomes that can alter the tumor microenvironment. We have previously shown that mutant KRAS induces EGFR-ligand trafficking to exosomes and drastically alters exosomal protein contents,...
ORGANISM(S): Homo sapiens 
2015-08-28 | E-GEOD-67004 | biostudies-arrayexpress
ProteomicsIdentification of KRas interactors in pancreatic cancer cell lines growing on matrix of different rigidities
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. T...
ORGANISM(S): Homo sapiens (Human) 
2026-09-14 | PXD069885 | Pride
Lc-ms-ms Integrins Pancreatic cancer. pdac Mass spectrometry Kras 
ProteomicsMutant KRAS-associated proteome is mainly controled by exogenous factors
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 ...
ORGANISM(S): Homo sapiens (Human) 
2022-04-06 | PXD030551 | Pride
Mutant kras  colorectal cancer  cancer associated-fibroblasts  proteomic analysis 
TranscriptomicsRNA-seq to investigate impact of treatment of KRAS mutant A549 lung adenocarcinoma cells with the multi-ERBB inhibitor Neratinib
KRAS mutation is widely presumed to confer independence from upstream RTK signalling, however emerging evidence from mouse models of lung cancer suggests that ERBB RTKs may amplify signalling through RAS isoforms and participate in mutant RAS-driven lung cancer. This is one of 3 datasets where we e...
ORGANISM(S): Homo sapiens 
2018-06-01 | E-MTAB-6483 | biostudies-arrayexpress
TranscriptomicsRNA-seq to investigate impact of treatment of KRAS mutant NCI-H2009 lung adenocarcinoma cells with the multi-ERBB inhibitor Neratinib
KRAS mutation is widely presumed to confer independence from upstream RTK signalling, however emerging evidence from mouse models of lung cancer suggests that ERBB RTKs may amplify signalling through RAS isoforms and participate in mutant RAS-driven lung cancer. This is one of 3 datasets where we e...
ORGANISM(S): Homo sapiens 
2018-06-01 | E-MTAB-6486 | biostudies-arrayexpress
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