Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RNA-seq profiling of C2C12 lung cancer-related fatigue cellular models treated with elesclomol and sorafenib

ABSTRACT: This bulk RNA-seq study profiles differentiated C2C12 myotubes in a lung cancer-related fatigue (LCaRF) cellular model under control conditions and after combined elesclomol and sorafenib treatment. The experiment was designed to identify transcriptional changes associated with ferroptosis inducer-enhanced copper ionophore stress, cuproptosis-related responses, mitochondrial dysfunction, and redox-stress pathways.

ORGANISM(S): Mus musculus

PROVIDER: GSE337532 | GEO | 2026/08/19

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

RNA-seq profiling of C2C12 lung cancer-related fatigue cellular models treated with elesclomol and sorafenib

Project description:RNA-seq profiling of C2C12 lung cancer-related fatigue cellular models treated with elesclomol and sorafenib

| PRJNA1490235 | ENA

Quantitative proteomics of HT-1080 cells exposed to single-atom engineered graphene derivatives versus copper ionophore elesclomol and glutathione peroxidase 4 inhibitor RSL3

Project description:This dataset presents a comparative proteomic analysis of the human fibrosarcoma cell line HT-1080 in response to treatment with nitrogen-doped graphene acid (NGA) and the single atom engineered derivatives, NGA-Fe3+ and NGA-Cu2+. To further investigate the role of metal-induced cell death pathways, cells were exposed to elesclomol, a well-known copper ionophore, and RSL3, a ferroptosis activating compound. The main objective was to characterize the proteomic alterations associated with single atom engineered NGA to elucidate potential mechanisms of action. We also examined the effects of elesclomol and RSL3 to provide reference datasets for copper-induced cytotoxicity (aka cuproptosis) and ferroptosis, respectively. This dataset provides insights into the cellular responses triggered by NGA and its derivatives and how these materials impinge on regulated cell death pathways.

2026-02-02 | PXD067483 | Pride

AKT1 confers tumor resistance to cuproptosis by phosphorylating FDX1

Project description:Cuproptosis, a recently defined copper-dependent cell death, remains largely unexplored in tumor therapies, particularly in breast cancer. Our study demonstrates that triple-negative breast cancer (TNBC) bears a relative elevated copper levels and exhibit resistance to cuproptosis. Mechanistically, cooper activates AKT1 signaling pathway, which inhibits cuproptosis by directly phosphorylating ferredoxin-1 (FDX1), a key regulator involved in cuproptosis. AKT1-mediated FDX1 phosphorylation abrogates FDX1-induced cuproptosis and aerobic respiration, accompanied by promoting glycolysis. Consequently, combination of AKT1 inhibitors MK2206 and the copper ionophore elesclomol (ES) synergistically inhibits TNBC tumorigenesis both in vitro and in vivo. In summary, our findings uncover a critical mechanism underlying TNBC resistance to cuproptosis and propose a potential therapeutic approach for TNBC.

2025-05-07 | PXD058176 | Pride

Isocitrate Dehydrogenase 1 Primes Group-3 Medulloblastomas For Cuproptosis

Project description:MYC-driven Group-3 medulloblastomas (MB) are malignant pediatric brain cancers without cures. To define actionable metabolic dependencies, we identified upregulationof dihydrolipoyl transacetylase (DLAT), the E2-subunit of pyruvate dehydrogenasecomplex (PDC) in a subset of Group-3 MB with poor prognosis. DLAT was induced by c-MYC and targeting DLAT lowered TCA-cycle metabolism and glutathione synthesis in Group-3 MB cells. We also noted upregulation of isocitrate dehydrogenase 1 (IDH1) in Group-3 MB. Remarkably, genetic and pharmacologic suppression of IDH1 epigenetically reduced c-MYC and downstream DLAT levels. DLAT is a central regulator of cuproptosis, a copper-dependent cell death mechanism induced by the copper ionophore elesclomol. DLAT expression in Group-3 MB cells correlated with increased sensitivity to cuproptosis. Elesclomol was CNS-penetrant and suppressed tumor growth in vivo in Group-3 MB animal models. Our data uncover an IDH1/c-MYC dependent vulnerability that regulates DLAT levels and can be targeted to kill Group-3MB by cuproptosis.

2025-04-10 | GSE278880 | GEO

Next-generation sequencing is useful for quantitative analysis of the transcriptome of HMME-RGD@C3F8 NBs under low-frequency ultrasound irradiation combined with Elesclomol-Cu treated and untreated HCC cells

Project description:Hepatocellular carcinoma has a hidden onset and is often found at an advanced stage clinically. Moreover, because it is insensitive to radiotherapy and chemotherapy, its treatment is often difficult. In this study, we constructed nanobubbles loaded with sonosensitizer HMME and tumor-targeting peptide RGD (HMME-RGD@C3F8 NBs) combined with cuproptosis inducer Elesclomol-Cu to achieve sonodynamic/cuproptosis combined therapy for hepatocellular carcinoma (HCC). Furthermore, to explore the mechanism of the enhanced anti-tumor efficacy of synergistic sonodynamic/cuproptosis therapy, RNA sequencing was performed.

2025-08-01 | GSE274917 | GEO

NUDT21 lactylation reprograms alternative polyadenylation to promote cuproptosis resistance

Project description:Alternative polyadenylation (APA) serves as a critical mechanism for shaping transcriptome diversity and modulating cancer therapeutic resistance. While lactate is a well-established metabolic signal in cancer progression, its role in APA regulation remains unclear. Here, we demonstrate that L-lactate-induced lactylation of NUDT21 drives transcriptomic reprogramming through APA modulation. NUDT21 lactylation enhances its interaction with CPSF6, facilitating CFIm complex formation and inducing 3′ untranslated region (UTR) lengthening of FDX1. Extension of the FDX1 3′ UTR attenuates its protein output, thereby conferring resistance to cuproptosis in esophageal squamous cell carcinoma (ESCC). Furthermore, we identify AARS1 as the lactylation “writer” catalyzing NUDT21 K23 lactylation, and HDAC2 as its enzymatic “eraser”. Clinically, elevated LDHA and NUDT21 levels correlate with reduced FDX1 expression and worse prognosis in ESCC patients. Notably, combined targeting of the lactate-NUDT21-FDX1-cuproptosis axis with the clinical LDHA inhibitor stiripentol and the copper ionophore elesclomol synergistically suppressed tumor growth. Collectively, our work identifies lactylated NUDT21 as a critical factor linking cellular metabolism to APA and proposes a promising therapeutic strategy for ESCC treatment.

2025-05-12 | GSE284372 | GEO

Transcription profiling of human Hs 294T cells treated with elesclomol alone or in combination with paclitaxel compared to DMSO treated

Project description:We used microarrays to detail gene expression changes in Hs 294T human melanoma cells after treatment with elesclomol alone, or in combination with paclitaxel, to aide in identifing the mechnism of action of elesclomol. Experiment Overall Design: Hs 294T human melanoma cells were grown in vitro. They were seeded at a low density and were left untreated, treated with the vehicle, treated with elesclomol, treated with paclitaxel, or treated in combination with both elesclomol and paclitaxel. They were incubated for 6 hours before harvesting.

2008-06-19 | E-GEOD-11550 | biostudies-arrayexpress

Hs 294T Cells Treated with Elesclomol Alone or in Combination with NAC Compared to DMSO Treated

2008-05-29 | GSE11551 | GEO

Hs 294T Cells Treated with Elesclomol Alone or in Combination with Paclitaxel Compared to DMSO Treated

2008-05-29 | GSE11550 | GEO

Transcription profiling of human 294T Cells treated with elesclomol alone or in combination with NAC compared to DMSO treated

Project description:We used microarrays to detail gene expression changes in Hs 294T human melanoma cells after treatment with elesclomol alone, or in combination with NAC, to aide in identifing the mechnism of action of elesclomol. Experiment Overall Design: Hs 294T human melanoma cells were grown in vitro. They were seeded at a low density and were left untreated, treated with the vehicle, treated with elesclomol, treated with NAC, or treated in combination with both elesclomol and NAC. The cells treated with NAC were given the NAC 30 minutes prior to additional treatments. They were incubated for 6 hours before harvesting.

2008-06-18 | E-GEOD-11551 | biostudies-arrayexpress