Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

The effects of nintedanib combined with radiation on gene transcription in the MC38 cell line

ABSTRACT: Nintedanib, a small molecule tyrosine kinase inhibitor, has been approved for patients with NSCLC who progressed following first-line chemotherapy. However, there are relatively few related studies on the treatment strategy of nintedanib combined with radiotherapy. This study aims to explore the effectiveness and mechanism of nintedanib combined with radiotherapy in both in vivo and in vitro experiments.

ORGANISM(S): Mus musculus

PROVIDER: GSE297011 | GEO | 2025/05/31

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

The effects of nintedanib combined with radiation on gene transcription in the MC38 cell line

Project description:The effects of nintedanib combined with radiation on gene transcription in the MC38 cell line

| PRJNA1262380 | ENA

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 | GSE182833 | GEO

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

2023-04-13 | GSE218575 | 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

| PRJNA904345 | ENA

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

Epigenome analyses reveal histone H4K20me3 and radiation related genes in NSCLC cell

Project description:Purpose: Radiotherapy is useful for non-small cell lung cancer (NSCLC) patients who cannot be treated surgically. Modification of histone proteins also occurs during radiotherapy, and affects gene expression. In this study, we assessed the effects of radiotherapy on histone H4K20me3 in NSCLC cells. Methods: NCI-H460 NSCLC cell line were subjected to gamma irradiation. To reveal H4K20me3-related genes, we conducted chromatin immunoprecipitation(ChIP) and ChIP-sequencing. Results: We evaluated the H4K20me3-related genes through ChIP-sequencing.

2020-05-12 | GSE133519 | GEO

Transcriptome analyses reveal epigenetic and radiation related genes in NSCLC cell

Project description:Purpose: Radiotherapy is useful for non-small cell lung cancer (NSCLC) patients who cannot be treated surgically. Modification of histone proteins occurs during radiotherapy, and affects gene expression.In this study, we assessed the effects of radiotherapy on histone modification via 3-deazaneplanocin A (DZNep) in NSCLC cells. Methods: NCI-H460 NSCLC cell line were subjected to gamma irradiation. To reveal histone modification reagent DZNep targeted genes, we conducted mRNA-sequencing. Results: We evaluated the epigenetic regulation of autophagy-related genes by DZNep through mRNA-sequencing, and we identified genes that are differentially expressed upon irradiation, including a candidate histone modification target gene.

2020-05-12 | GSE133518 | GEO

Radiation combined with KRAS-MEK inhibitors enhances anticancer immunity in KRAS-mutated tumor models [CT26 RNA-seq]

Project description:KRAS mutation is a common driver in solid tumors, and KRAS-mutated tumors are relatively resistant to radiotherapy. Therefore, we investigated the combined effect of radiation and KRAS-MEK inhibitors (AMG510 and trametinib) in KRAS-mutated tumors.

2022-10-01 | GSE209765 | GEO

Radiation combined with KRAS-MEK inhibitors enhances anticancer immunity in KRAS-mutated tumor models [LLC RNA-seq]

2022-10-01 | GSE209766 | GEO