Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Nintedanib inhibits the VEGFR-ERK signaling pathway in human KRAS-mutated cancer cells

ABSTRACT: To investigate the effect of Nintedanib in KRAS mutant, we have emoloyed whole genomic microarray expression profiling using HPNE cells

ORGANISM(S): Homo sapiens

PROVIDER: GSE312012 | GEO | 2026/01/31

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Nintedanib inhibits the VEGFR-ERK signaling pathway in human KRAS-mutated cancer cells

Project description:Nintedanib inhibits the VEGFR-ERK signaling pathway in human KRAS-mutated cancer cells

| PRJNA1372052 | ENA

Proteomics of KRAS mutated and non-transformed pancreas cells treated with ethanol

Project description:The goal for this study was to determine the effects of ethanol on pancreas cells and examine how ethanol influences protein expression in non-transformed and mutant KRAS cells. We performed TMT-labeled proteomics of non-transformed (hTERT-HPNE E6/E7) and KRAS mutated (hTERT-HPNE E6/E7/K-RasG12D) human pancreas cell lines following 6 months of 100 mM ethanol treatment.

2022-05-19 | PXD030180 | Pride

The role of UHRF1 in KRAS-mutated pancreatic cancer cells

Project description:To investigate the effect of UHRF1 in KRAS mutant on gene expression, we have emoloyed whole genomic microarray expression profiling using PL5 cells

2026-04-30 | GSE325201 | GEO

Mutant Kras- and p16-Regulated NOX4 Activation Overcomes Metabolic Checkpoints in Development of Pancreatic Ductal Adenocarcinoma

Project description:That mutational activation of Kras and inactivation of p16 are two signature genetic alterations required for development of PDAC. To elucidate the downstream pathways activated by oncogenic Kras and inactivated p16 in human pancreatic tumorigenesis, we profiled gene expression in HPNE/Kras/shp16 and HPNE/Kras cells using cDNA microarray analysis.

2016-11-03 | GSE89422 | GEO

SORL1 is a mediator of KRAS driven oncogenesis in multiple myeloma

Project description:To investigate the effect of SORL1 in KRAS mutant, we have emoloyed whole genomic microarray expression profiling using Sachi-KRAS-G12A cells

2026-03-31 | GSE315013 | GEO

Nintedanib induces senolytic effect via STAT3 inhibition

Project description:Selective removal of senescent cells, or the concept of senolytic therapy, has been proposed to be a potent strategy for overcoming age-related diseases and even reversing aging. We found that nintedanib, a tyrosine kinase inhibitor, selectively induced cell death in primary human diploid fibroblasts undergoing replicative senescence. Similar to ABT263, a well-known senolytic agent, nintedanib triggered intrinsic apoptosis in senescent cells. Additionally, at the concentration producing the senolytic effect, nintedanib arrested the cell cycle of nonsenescent cells in the G1 phase without cytotoxicity. Interestingly, compared with ABT263, nintedanib showed a different mode of activating caspase-9 in the intrinsic apoptotic pathway, in that nintedanib did not suppress the levels of Bcl-2 family proteins in senescent cells. In more detail, nintedanib suppressed the activation of the JAK2/STAT3 pathway, which caused drug-induced cell death in senescent cells. STAT3 knockdown in senescent cells also induced caspase activation. Moreover, nintedanib reduced the number of senescent cells stained based on senescence-associated β-galactosidase activity and airway resistance in a mouse model of bleomycin-induced lung fibrosis. Overall, we identified that nintedanib could be used as a new senolytic agent and that inhibiting STAT3 could be a potential approach for inducing selective cell death in senescent cells. Our findings will pave the way for expanding senolytic toolkits in response to various aging statuses and age-related diseases.

2022-09-06 | GSE210020 | GEO

Transcriptomic analysis of Nintedanib, Alpelisib and Nintedanib;Alpelisib treated bladder tumors

Project description:Nintedanib is a potent anti-fibrotic angio-kinase inhibitor, which has shown clinical efficacy in combination with chemotherapy in locally advanced muscle invasive BC patients. Nintedanib inhibits Fibroblast Growth Factor receptors (FGFRs), validated targets in patients with BC harboring FGFR3/2 genetic alterations. Here, we aimed at studying its mechanisms of action to understand therapy their combination (n=4). Reads were mapped separately against the human and mouse genomes to differentiate tumor vs. stromal expression changes

2023-04-13 | GSE218575 | GEO

Transcriptomic analysis of Nintedanib, Alpelisib and Nintedanib;Alpelisib treated bladder tumors

2023-04-13 | GSE182833 | GEO

RNA-seq Analysis of KRAS Mutant HPNE Pancreatic Ductal Epithelial Cells

Project description:KRAS mutations drive pancreatic cancer initiation by reprogramming cellular signaling and the tumor microenvironment. Here, we investigate the early transcriptional impact of distinct KRAS mutants in a non-cancerous pancreatic epithelial context. Using RNA-seq, we profiled HPNE cells engineered with inducible KRAS variants (G12D, G12V, G12R, Q61H, Q61K, Q61R) compared to wild-type KRAS (WT) following 24-hour induction. This comparative analysis reveals that KRAS mutations differentially regulate immune and extracellular matrix remodeling pathways, with G12D and Q61R/H mutants driving pro-inflammatory signaling, while G12R and Q61k exhibits distinct transcriptional suppression. These findings highlight the mutation-specific transcriptional landscapes of KRAS in pancreatic epithelial cells and provide insight into the early events shaping the pancreatic tumor microenvironment.

2026-05-12 | GSE295683 | GEO

Transcriptomic analysis of Nintedanib, Alpelisib and Nintedanib Alpelisib treated bladder tumors

Project description:Transcriptomic analysis of Nintedanib, Alpelisib and Nintedanib Alpelisib treated bladder tumors

| PRJNA758030 | ENA