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Single cell RNAseq of Tumour Endothelial Cell from response or partial response tumors to Doxorubicin treatment

ABSTRACT: To investigate the effects of Dox treatment on Tumor Endothelial Cell (TEC) dynamics at single-cell resolution, we carried out 10X single-cell RNA sequencing. Doxorubicin exposure triggers a significant reprogramming of the tumour vasculature, substantially altering the angiocrine landscape and shaping treatment outcomes

ORGANISM(S): Mus musculus

PROVIDER: GSE314267 | GEO | 2026/07/01

REPOSITORIES: GEO

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Tumour endothelial cells transcriptomics in response to Doxorubicin treatment.

Project description:Despite its established role in breast cancer treatment, Doxorubicin remains a challenge in breast cancer treatment as its long-term success is prevented by adaptive resistance mechanisms that extend beyond cancer cell intrinsic alterations. Our study in a MMTV-PyMT-driven mouse breast cancer model reveals that prolonged Doxorubicin exposure triggers a significant reprogramming of the tumour vasculature, substantially altering the angiocrine landscape and shaping treatment outcomes.

2026-07-01 | GSE311784 | GEO

Transcriptome changes in human PSC-derived cardiomyocytes induced by doxorubicin II

Project description:Doxorubicin (DOX) is one of the most effective chemotherapeutic agents for various types of cancers. However, DOX often causes cardiotoxicity referred to as DOX-induced cardiomyopathy (DIC). In this experiment, transcriptome changes induced by doxorubicin were examined in human PSC-derived cardiomyocytes.

2026-02-08 | GSE255505 | GEO

Magnetic-Targeted Doxorubicin in Treating Patients With Cancer Metastatic to the Liver

Project description:MTC-DOX is Doxorubicin or DOX, a chemotherapy drug, that is adsorbed, or made to "stick", to magnetic beads (MTCs). MTCs are tiny, microscopic particles of iron and carbon. When DOX is added to MTCs, DOX attaches to the carbon part of the MTCs. MTC-DOX is directed to and deposited in the area of a tumor, where it is thought that it then "leaks" through the blood vessel walls. Once in the surrounding tissues, it is thought that Doxorubicin becomes "free from" the magnetic beads and will then be able to act against the tumor cells. The iron component of the particle has magnetic properties, making it possible to direct MTC-DOX to specific tumor sites in the liver by placing a magnet on the body surface. It is hoped that MTC-DOX used with the magnet may target the chemotherapy drug directly to liver tumors and provide a treatment to patients with cancers that have spread to the liver.

| 2007949 | ecrin-mdr-crc

Gene Expression upon Doxorubicin Treatments

2010-07-15 | GSE17115 | GEO

The gut microbiota-butyrate axis restores cardiomyocyte autophagy to alleviate Doxorubicin-induced cardiotoxicity

Project description:AbstractBackground Doxorubicin (DOX), an anthracycline chemotherapeutic agent, is widely used for treating various malignancies. However, its clinical application is limited by dose-dependent cardiotoxicity (DOX-induced cardiotoxicity, DIC). Recent studies have shown that the gut microbiota and its metabolites may be involved in the occurrence and development of cardiovascular diseases through the 'gut-microbiota-heart axis'. Especially，doxorubicin may affect the structure and function of the gut microbiota due to its potential antimicrobial properties and its gut-damaging side effects, but the molecular mechanisms through which gut microbiota affects DIC remain poorly understood.Results The results of 16S rRNA gene amplicon sequencing of fecal samples showed that the gut microbiota structure of the C57BL/6 DIC model mice changed. The depletion of gut microbiota by antibiotics partially improved DIC. Fecal microbiota transplantation (FMT) from DOX-treated donors impaired cardiac structure and function in recipient mice. Conversely, control-donor FMT significantly alleviated DOX-induced cardiac dysfunction, whether co-administered or given post-modeling. Mechanistically, we analyzed the metabolomics of fecal samples from mice after DOX administration and identified butyric acid (BA) as a key metabolite. Further experiments have shown that after BA treatment, the fatty acid oxidation levels impaired by DOX was restored meanwhile the glycolysis was inhibited. Besides, it was preliminarily confirmed that this metabolic alteration affects 4-hydroxynonenal (4HNE) and autophagy levels, which in turn affects DIC.Conclusions The gut microbiota-butyrate axis restores fatty acid oxidation and normalizes glycolytic activity, further enhancing 4-HNE-mediated autophagy as a therapeutic strategy against DIC.Keywords Doxorubicin, Gut microbiota, Cardiotoxicity, Butyric acid

2025-09-16 | MTBLS12997 | MetaboLights

Fibroblast-driven transcriptional reprogramming in response to doxorubicin in heterotypic melanoma spheroids

Project description:Bulk RNA-sequencing was used to compare the transcriptional response to doxorubicin (DOX) between two multicellular melanoma spheroid models: a baseline model composed of B16.F10 melanoma cells, 2H11 endothelial cells, and bone marrow-derived macrophages (BEM), and a fibroblast-containing counterpart (BEMF) additionally incorporating primary murine dermal fibroblasts. Spheroids of each model were exposed for 48 h to their respective IC30 concentration of doxorubicin (0.56 microM for BEM; 0.79 microM for BEMF) or left untreated as controls, in two independent biological replicates per model/treatment combination. RNA-seq was performed to identify differentially expressed genes associated with fibroblast-dependent modulation of the doxorubicin response in melanoma spheroids.

2026-06-30 | GSE336658 | GEO

Endothelial transcription factor EB protects against doxorubicin-induced endothelial toxicity and cardiac dysfunction

Project description:Doxorubicin (DOX) has been demonstrated to induce cardiovascular toxicity in cancer survivors. Endothelial cell dysfunction is recoginized to play a critical role in the onset and severity of cardiotoxicity associated with DOX. Endothelial TFEB protects against EC damage and cardiac dysfunction. Cardiac single cells isolated from vehicle and doxorubicin treated wild type and EC-Tfeb Tg mice were collected for scRNA-seq analysis.

2025-12-18 | GSE285475 | GEO

Gene Expression upon Doxorubicin Treatments

Project description:Murine C26 tumor xenografts displayed different responses to the treatments of PBS, Doxorubicin (Dox), and chimeric polypeptide (CP)-Dox conjugates. We used microarrays to globally study gene expression underlying these different responses and identified distinct classes of up-regulated or down-regulated genes upon treatment. C26 murine colon carcinoma xenografts were analyzed at 48 hours after treatment with CP-Dox, free Dox, and PBS (control). This study involved four replicates of each treatment.

2010-07-15 | E-GEOD-17115 | biostudies-arrayexpress

The Secretome of Human Neonatal Mesenchymal Stem Cells Modulates Doxorubicin-induced Cytotoxicity: Impact in Non-tumour Cells

Project description:Breast cancer remains one of the leading causes of death in women, being the chemotherapeutic agent doxorubicin (Dox) among the most widely standard chemotherapy options for its treatment. However, its effective use has been severely limited owing to its well-documented cardiotoxic side effect that can lead to heart failure in a subset of patients. We have previously shown that a specific population of mesenchymal stem cells (MSCs) present immunomodulatory and regenerative properties, mainly granted by its secretome (CM), whose potential was improved when produced under 3D conditions. In cancer, the role of MSCs is still contradictory, with literature reporting both cancer promoting and suppressive effects. Therefore, we aimed at determining the effect of concomitant exposure of Dox with CM from 3D (CM3D) and 2D (CM2D) MSC cultures in breast cancer cells (MDA-MB-231) and in non-tumour breast epithelial cells (MCF10A) and differentiated AC16 cardiomyocytes. As such, the whole secretome was obtained by collecting and concentrating the culture media conditioned by MSCs in 2D (CM2D) and 3D (CM3D). A Ge-LC-MS/MS proteomic analysis revealed that CM3D effects may be linked to MSC cytoprotection and tumour development, namely through regulation of cell proliferation (CAPN1, CST1, LAMC2, RANBP3), migration (CCN3, MMP-8, PDCD5), invasion (TIMP-1/2), oxidative stress (AIFM1, CD9, GSR) and inflammation (ANXA5, CDH13, GDF-15). Overall, MSC-derived CM3D decreased Dox-induced cytotoxic effects on non-tumour breast cells and cardiomyocytes, without compromising Dox chemotherapeutic nature, highlighting the potential use of CM3D as an adjuvant in chemotherapy to reduce off-target side effects.

2022-02-17 | PXD029795 | Pride

The expression profiles of human lymphoma H9 cells after exposure to doxorubicin

Project description:doxorubicin is commonly used for hematological malignancies. Since some of PTCL patients resistance to dox and die due to refractory disease or relapse, enhanced knowledge about drug response mechanisms is required to improve treatment outcome. we found an increased expression of HDAC3 in T lymphoma H9 cells following dox exprosure, we compared the gene expression profiles of H9 cells pre/post treated with doxorubicin to explore the potential mechanism of the high expression of HDAC3

2024-04-18 | GSE260756 | GEO

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