Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Effect of depletion of HMOX1 on gene expression of AsPC-1 cells.

ABSTRACT: Pancreatic ductal adenocarcinoma (PDAC) is one of the most malignant tumors. Endoplasmic reticulum stress plays an essential role in PDAC progression. Here, we aim to identify the ERS-related genes in PDAC and build reliable risk models for diagnosis, prognosis and immunotherapy response of PDAC patients. We report HMOX1 as an important gene of ER stress related-signature we established in PDAC. The depletion of HMOX1 results in tumor growth inhibition. Our data lay the foundation for further investigating the potential mechanism.

ORGANISM(S): Homo sapiens

PROVIDER: GSE241352 | GEO | 2023/08/24

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Effect of depletion of HMOX1 on gene expression of AsPC-1 cells.

Project description:Effect of depletion of HMOX1 on gene expression of AsPC-1 cells.

| PRJNA1007732 | ENA

Inhibition of HMOX1 alleviates diabetic cardiomyopathy by targeting ferroptosis

Project description:Diabetic cardiomyopathy (DCM) is an important complication of chronic diabetes mellitus (DM). However, its pathogenesis and pathologic process have not been fully elucidated. This study was aimed to investigate the role of ferroptosis in the pathogenesis of DCM and clarify the effect of HMOX1 on DCM by targeting ferroptosis. DCM mouse model was constructed by high fat diet (HFD) feeding and streptozotocin (STZ). injection.

2023-08-28 | GSE241166 | GEO

Inhibition of HMOX1 alleviates diabetic cardiomyopathy by targeting ferroptosis

Project description:Inhibition of HMOX1 alleviates diabetic cardiomyopathy by targeting ferroptosis

| PRJNA1006668 | ENA

IFI16-mediated cellular senescence drives HMOX1-dependent evasion of ferroptosis and radioresistance in glioblastoma

Project description:Glioblastoma multiforme (GBM) is a persistent challenge in oncology due to its aggressive nature and limited survival. Despite various therapeutic strategies, the recurrence of GBM still exists, driven by the complex cellular diversity and evolutionary dynamics during the treatment process. This study established a radioresistant GBM cell model through repeated exposure to ionizing radiation and revealed a distinct manifestation of cellular senescence of these cells. The comprehensive genomic and transcriptomic analyses identified that IFI16, as a critical driver of cellular senescence, contributed to the radioresistance of GBM. Mechanistically, IFI16 was involved in orchestrating HMOX1 transcription thereby attenuating ferroptosis after irradiation. HMOX1 limited lipid peroxidation, reactive oxygen species (ROS) production, and intracellular Fe2+ content following irradiation, thus effectively counteracting ferroptosis in GBM. Furthermore, IFI16 interacted with the transcription factors JUND and SP1 through its pyrin domain, robustly facilitating HMOX1 expression, further inhibiting ferroptosis and enhancing radioresistance in GBM cells. Notably, glyburide, an anti-aging agent, effectively disrupted IFI16 function and thus enhanced ferroptosis and radiosensitivity. By specifically targeting the pyrin domain of IFI16, glyburide emerged as a potential therapeutic agent against GBM radioresistance. In conclusion, these novel findings underscored the central role of IFI16 in GBM radioresistance and offered promising avenues for innovative therapeutic interventions against GBM radiosensitivity

2024-12-25 | GSE274090 | GEO

Melanoma bone metastasis-induced osteocyte ferroptosis via the HIF1α-HMOX1 axis.

Project description:Osteocytes are the main cells in mineralized bone tissue. Elevated osteocyte apoptosis has been observed in lytic bone lesions of patients with multiple myeloma. However, their precise contribution to bone metastasis remains unclear.Here, we investigated the pathogenic mechanisms driving melanoma-induced osteocyte death. Both in vivo models and in vitro assays were combined with untargeted RNA sequencing approaches to explore the pathways governing melanoma-induced osteocyte death. We could show that ferroptosis is the primary mechanism behind osteocyte death in the context of melanoma bone metastasis. HMOX1 was identified as a crucial regulatory factor in this process, directly involved in inducing ferroptosis and affecting osteocyte viability. We uncover a non-canonical pathway that involves excessive autophagy-mediated ferritin degradation, highlighting the complex relationship between autophagy and ferroptosis in melanoma-induced osteocyte death. In addition, HIF1α pathway was shown as an upstream regulator, providing a potential target for modulating HMOX1 expression and influencing autophagy-dependent ferroptosis. In conclusion, our study provides insight into the pathogenic mechanisms of osteocyte death induced by melanoma bone metastasis, with a specific focus on ferroptosis and its regulation. This would enhance our comprehension of melanoma-induced osteocyte death.

2024-11-24 | GSE276370 | GEO

Melanoma bone metastasis-induced osteocyte ferroptosis via the HIF1α-HMOX1 axis II

2024-11-24 | GSE276373 | GEO

Melanoma bone metastasis-induced osteocyte ferroptosis via the HIF1α-HMOX1 axis.

Project description:Melanoma bone metastasis-induced osteocyte ferroptosis via the HIF1α-HMOX1 axis.

| PRJNA1156790 | ENA

Quantification of oxidative stress-related proteins using MRM approach in atherosclerosis-related and non-related to chronic kidney disease

Project description:The aim of MRM analysis of selected oxidative stress-related proteins, including MPO, CERu, sTNF, SOD3, HMOX1, PON1, GPX3, NOS2, CAT and IFNG was to investigate changes in plasma samples from patients at different stages of atherosclerosis-related to chronic kidney disease, classical atherosclerosis as well as in comparison with healthy controls.

2024-01-23 | PXD041820 | Pride

Melanoma bone metastasis-induced osteocyte ferroptosis via the HIF1α-HMOX1 axis II

Project description:Melanoma bone metastasis-induced osteocyte ferroptosis via the HIF1α-HMOX1 axis II

| PRJNA1156793 | ENA

Expression data of AsPC-1 and MIA Paca-2 cell lines cultured in nutrient deprivation

Project description:Pancreatic ductal adenocarcinoma (PDAC) aggressiveness largely relies on its capability to thrive and progress in a highly desmoplastic microenvironment with limited nutrients. We used microarrays to identify genes potentially dysregulated by nutrient deprivation in two different PDAC cell lines

2023-07-17 | GSE237164 | GEO

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