Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Effect of cisplatin on gene expression of human umbilical vein endothelial cells

ABSTRACT: Cisplatin (DDP) is a widely used chemotherapeutic agent that induces apoptosis in various cancer cells, but its effects on endothelial cells such as HUVEC (Human Umbilical Vein Endothelial Cells) are less well understood. This study aims to explore the transcriptional response of HUVEC cells to cisplatin treatment. RNA-seq analysis was performed to identify differentially expressed genes following cisplatin stimulation, providing insights into the molecular mechanisms underlying the cellular response to chemotherapy in endothelial cells. The results highlight key pathways and genes involved in the stress response, apoptosis, and cellular survival in HUVEC cells upon cisplatin treatment.

ORGANISM(S): Homo sapiens

PROVIDER: GSE275662 | GEO | 2025/07/01

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Effect of cisplatin on gene expression of human microvascular endothelial cells

Project description:Cisplatin (DDP) is a widely used chemotherapeutic agent that induces apoptosis in various cancer cells, but its effects on endothelial cells such as HMEC-1 (Human Microvascular Endothelial Cell line-1) are less well understood. This study aims to explore the transcriptional response of HMEC-1 to cisplatin treatment. RNA-seq analysis was performed to identify differentially expressed genes following cisplatin stimulation, providing insights into the molecular mechanisms underlying the cellular response to chemotherapy in endothelial cells. The results highlight key pathways and genes involved in the stress response, apoptosis, and cellular survival in HMEC-1 cells upon cisplatin treatment.

2025-07-01 | GSE275667 | GEO

Jinfukang enhances the pro-apoptotic activity of cisplatin via activation of AIFM2 in human lung cancer cells

Project description:Application of cisplatin (DDP) for treating lung cancer is restricted due to its toxicity and drug resistance. In this study, we aimed to examine whether Jinfukang (JFK), an effective herbal medicine against lung cancer, enhances DDP-induced cytotoxicity in lung cancer cells. Morphologically, we observed JFK increases DDP-induced pro-apoptosis in A549 cells in a synergistic manner. Transcriptome profiling analysis indicated that combination of JFK and DDP regulates genes involved in apoptosis-related signaling pathways. Moreover, we found the combination of JFK and DDP produces synergistic pro-apoptosis effect in other lung cancer cell lines NCI-H1975, NCI-H1650 and NCI-H2228. Particularly, we demonstrated AIFM2 is activated by the combined treatment of JFK and DDP, and partially mediate the synergistic pro-apoptosis effect. Collectively, this study gives the first evidence that activation of AIFM2 contributes to induction of pro-apoptosis by combined treatment with JFK and DDP in human lung cancer cells and provides an insight for its potential clinical application in lung cancer treatment.

2016-09-30 | E-MTAB-4671 | biostudies-arrayexpress

Combined Time Restricted Feeding and Cisplatin Enhance the Anti-tumor Effects in Cisplatin Resistant and -Sensitive Lung Cancer Cells

Project description:Combination therapy as an important treatment option for lung cancer has been attracting attention due to the primary and acquired resistance of chemotherapeutic drugs in the clinical application. In the present study, as a new therapy strategy, concomitant treatment with time-restricted feeding (TRF) plus cisplatin (DDP) on lung cancer growth was investigated in DDP-resistant and DDP-sensitive lung cancer cells. We first found that TRF significantly enhanced the drug susceptibility of DDP in DDP-resistant A549 (A549/DDP) cell line, illustrated by reversing the inhibitory concentration 50 (IC50) values of A549/DDP cells to normal level of parental A549 cells. We also found that TRF markedly enhanced DDP inhibition on cell proliferation, migration, as well as promoted apoptosis compared to the DDP-alone group in A549, H460 and A549/DDP cells lines. We further revealed that the synergistic anti-tumor effect of combined DDP and TRF was greater than that of combined DDP and simulated fasting condition (STS), a known anti-tumor cellular medium. Moreover, mRNA sequence analysis from A549/DDP cell line demonstrated the synergistic anti-tumor effect involved in upregulated pathways in p53 signaling pathway and apoptosis. Notably, compared with the DDP-alone group, combination of TRF and DDP robustly upregulated the P53 protein expression without mRNA level change by regulating its stability via promoting protein synthesis and inhibiting degradation, revealed by cycloheximide and MG132 experiments. Collectively, our results suggested that TRF in combination with cisplatin might be an additional novel therapeutic strategy for patients with lung cancer

2023-01-11 | GSE222187 | GEO

Expression profiling in Human Umbilical Vein Endothelial Cells (HUVEC)

Project description:Whole transcriptome gene expression profiling of Normal -(HUVEC) Human Umbilical Vein Endothelial Cells The HUVEC gene expression results analyzed in this study are further described in Kustermann S. et al. (2014) A real-time impedance based screening assay for drug induced vascular leakage.

2014-01-07 | GSE52044 | GEO

Proteomic response of human umbilical vein endothelial cells to histamine stimulation

Project description:Endothelial cells (HUVEC) were treated with histamine, the endogenous ligand of histamine receptors, for a global overview of its cellular effects. Changes of the intracellular and secreted proteomes were analyzed using shotgun proteomics. Furthermore, a selected set of proteins was quantified using parallel reaction monitoring.

2017-02-28 | MSV000080587 | MassIVE

m6A modification in cisplatin-resistant cells

Project description:We report the application of specific antibodies and high-throughput sequencing technologies (methylated RNA immunoprecipitation sequencing, MeRIP-seq) for high-throughput profiling of m6A modifications in NSCLC cisplatin resistant cells. We generated maps of m6A modified transcripts in A549 and A549/DDP cells. We find that the m6A level was significantly increased in A549/DDP cells compared to the A549 cells. We show that there was a close correlation between the m6A modification and cisplatin resistance.

2022-11-04 | GSE140020 | GEO

Exploring the Cytotoxic Mechanisms and Anticancer Potentials of Silver Nanoparticles in Cisplatin-Sensitive and -Resistant Lung Adenocarcinoma: Insights from Proteomic and Mice Xenograft Studies

Project description:Silver nanoparticles (AgNPs) have shown great potential as therapeutic agents due to their ability to cause apoptotic cell death in cancer cells. However, little knowledge is available regarding the underlying action mechanisms of AgNPs towards multi-drug resistant cancer cells. Herein, we employed quantitative proteomics to investigate the cytotoxic mechanisms of AgNPs on both cisplatin-sensitive (A549 cells) and -resistant (A549/DDP cells) human lung adenocarcinoma and to explore their potential anticancer abilities. We first performed cytotoxicity tests and found that AgNPs exert similar cytotoxic effects on A549 and A549/DDP cells. At the proteome level, A549 and A549/DDP cells responded to AgNPs distinctively and similarly by causing cell apoptosis via upregulating RNA metabolism, suppressing VEGF siganling pathway, repressing p53-mediated pathways, promoting cell cycle arrest, etc. Additionally, AgNPs remarkably induced ROS generation in A549 and A549/DDP cells. The mitotoxicity results further confirmed the effectiveness of AgNPs in hampering mitochondrial function and respiration in A549 and A549/DDP cells. Overall, our investigations showed that AgNPs could effectively induce cell deaths in human lung adenocarcinoma cells regardless of their sensitivities to cisplatin, suggesting that AgNPs could be potentially used in biomedical aspects as an anticancer agent in alleviating the problem of acquired drug resistance in chemotherapy.

2025-05-30 | PXD064272 | Pride

Effect of cisplatin on gene expression of human umbilical vein endothelial cells

Project description:Effect of cisplatin on gene expression of human umbilical vein endothelial cells

| PRJNA1152537 | ENA

Integration of metabolomics and transcriptomics to reveal metabolic characteristics and key targets associated with cisplatin resistance in non-small cell lung cancer

Project description:Continuous exposure to cisplatin can induce drug resistance to limit efficacy, however, the underlying mechanisms correlated to cisplatin resistance are still unclear. Drug-sensitive A549 cells and cisplatin-resistant A549/DDP cells were used to explore the potential metabolic pathways and key targets associated with cisplatin resistance by integrating untargeted metabolomics with transcriptomics. The results of comprehensive analyses showed that 19 metabolites were significantly changed in A549/DDP vs A549 cells, and some pathways had a close relationship with cisplatin resistance, such as the biosynthesis of aminoacyl-tRNA, glycerophospholipid metabolism, and glutathione metabolism. Moreover, transcriptomics analysis showed glutathione metabolism was also obviously affected in A549/DDP, which indicated that glutathione metabolism played an import role in the process of drug resistance. Meanwhile, transcriptomics analysis suggested the four enzymes related to glutathione metabolism - CD13, GPX4, RRM2B, and OPLAH - as potential targets of cisplatin resistance in NSCLC. Further studies identified the over-expressions of these four enzymes in A549/DDP. The elucidation of mechanism and discovery of new potential targets may help us have a better understanding of cisplatin resistance.

2019-08-12 | PXD013265 | Pride

Effect of neurotrophin receptor p75 (p75NTR) over-expression on the miRNAome of human umbilical vein endothelial cells

Project description:MicroRNAs (miRNAs) are small non-protein-coding RNAs that are incorporated into the RNA-induced silencing complex (RISC) and inhibit gene expression by regulating the stability and/or the translational efficiency of target mRNAs. p75NTR, which is scarcely present in healthy endothelial cells (ECs), becomes strongly expressed by capillary ECs after induction of peripheral ischemia in type-1 diabetic mice. p75NTR expression promotes endothelial cells apoptosis and inhibits angiogenesis. In order to identify miRNAs sub-sequentely modulated by p75NTR, miRNA expression profiles of human umbilical vein endothelial cells (HUVEC) over-expressing p75NTR were generated, allowing the identification of miRNAs modulated upon p75NTR up-regulation. HUVEC over-expressing p75NTR or Null (empty vector) were generated by adenoviral infection. miRNA expression profiles were then measured and miRNAs modulated upon p75NTR up-regulation were identified.

2014-01-11 | E-GEOD-53899 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data