Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RNASeq analysis of human Cal33 xenografts in nu/nu mice upon radiotherapy +/- metformin treatment

ABSTRACT: RNASeq analysis of human Cal33 xenografts in nu/nu mice upon radiotherapy +/- metformin treatment

PROVIDER: PRJNA770095 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR16287228.fastq.gz	Fastqsanger.gz
	SRR16287229.fastq.gz	Fastqsanger.gz
	SRR16287230.fastq.gz	Fastqsanger.gz
	SRR16287231.fastq.gz	Fastqsanger.gz
	SRR16287232.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 24

Similar Datasets

RNASeq analysis of human Cal33 xenografts in nu/nu mice upon radiotherapy +/- metformin treatment

Project description:Purpose: We aim to identify transciptional changes of Cal33 xenografts upon radiotherapy +/- metformin treatment in vivo Method: Cal33 cells were heterotopically transplanted onto NMRI nude mice and subjected to fractionated irradiation with 5x 2 Gy ± 5x 250 µg/g metformin treatment starting on d4 after inoculation. After 5 days of therapy, tumors were explanted, total RNA was extracted, and subjected to RNAseq analysis.

2022-01-11 | GSE185624 | GEO

RNASeq analysis of human ALDH- and ALDH+ DU145 xenografts in nu/nu mice upon radiotherapy treatment

Project description:Purpose: we aimed at identify and compare the transcriptional changes of ALDH- and ALDH+ DU145 xenografts upon radiotherapy treatment. Method: Xenografts were generated by injection of ALDH- and ALDH+ DU145 cells in male NMRI-Foxn1 nu/nu immune-deficient mice and subjected to fractionated irradiation to a final dose of 50 Gy. Tumors were excised and processed for total RNA extraction and RNAseq analysis.

2022-01-22 | GSE193963 | GEO

RNASeq analysis of human ALDH- and ALDH+ DU145 xenografts in nu/nu mice upon radiotherapy treatment

Project description:RNASeq analysis of human ALDH- and ALDH+ DU145 xenografts in nu/nu mice upon radiotherapy treatment

| PRJNA798623 | ENA

Transcription profiling by array to investigate the effect of combined external beam radiotherapy (photon or carbon) and 131I-Cetuximab endoradiotherapy in A431 xenograft tumors in mice

Project description:Subcutaneous A431 tumors in the right hind limb of NCr nu/nu mice were treated with 5 daily fractions of external beam radiotherapy (2 Gy photon or 1 Gy carbon per fraction), a single fraction of 7.2 MBq 131Iodine-labelled Cetuximab intravenously or a combination of the two. Untreated tumors served as controls. Mice were sacrificed and tumor tissue collected for expression profiling 5 days after endoradiotherapy of 1 week after the last fraction of external beam radiotherapy.

2023-12-08 | E-MTAB-6515 | biostudies-arrayexpress

Microglia coordinate the anti-tumor immune response to breast cancer brain metastasis [Foxn1 nu/nu 10X data]

Project description:We used single-cell RNA-sequencing to investigate the role of brain-resident microglia versus infiltrating cells in a mouse model of breast cancer brain metastasis (BCBM). We generated brain metastases with a cardiac-injection of the human triple-negative breast cancer cell line MDA-MB-231BR2 (231BR) into Foxn1 nu/nu mice and allowed tumors to grow in the brain for four weeks. We then compared astrocytes (ASCA2+CD45-) and myeloid cells (CD11b+CD45+) from these mice verses control Foxn1 nu/nu brains to find transcriptional changes associated with BCBM.

2023-09-01 | GSE147942 | GEO

Metformin enhanced the effect of a Ketogenic diet in MYCN amplified Neuroblastoma xenografts

Project description:Neuroblastoma (NB) is a childhood cancer in which the MYCN amplification is the most acknowledged marker of poor prognosis. MYCN-amplified NB cells showed to rely on both glycolysis and oxidative phosphorylation system (OXPHOS) for energy production . Previously, we revealed that a ketogenic diet (KD) slowed the tumor growth in MYCN NB xenografts, when combined with classical cytotoxic therapy cyclophosphamide (CP). Metformin (MET) is a compound that targets complex I of the OXPHOS system. Therefore, the aim of this study was to elucidate whether MET can enhance the anti-tumorigenic effects of a KD in NB. Our result indicated that MET decreasedcell proliferation andrespiration in NB cells in vitro. The combination of KD, MET and low dose of chemotherapyreduced also the tumor growth and improved survival in NB xenografts. GO enrichment analysis revealed fatty acid ß-oxidation as the most upregulated process resulting from the addition of MET to KD. The differential expression of CPT1A and of its direct regulator ACC might determine an unbalanced redox state and dictate the anti-tumor effect of the combination therapy in MYCN-amplified xenografts.

2024-09-30 | GSE236677 | GEO

The NAMPT inhibitor FK866 increases metformin sensitivity in pancreatic cancer cells

Project description:Pancreatic cancer (pancreatic ductal adenocarcinoma: PDAC) is one of the most aggressive neoplastic diseases. Metformin use was associated with reduced pancreatic cancer incidence or better survival in diabetics. Metformin has been shown to inhibit PDAC cells survival and growth in vitro and in vivo. However, clinical trials using metformin failed to decrease pancreatic cancer progression in patients, raising important questions about molecular mechanisms that protect tumor cells from the antineoplastic activities of metformin. We confirm that metformin acts through inhibition of mitochondrial complex I, decreasing the NAD+/NADH ratio and that NAD+/NADH homeostasis determines metformin sensitivity in several cancer cell lines. Metabolites that can restore the NAD+/NADH ratio turned PDAC cells resistant to metformin. In addition, metformin treatment of PDAC cell lines induced a compensatory NAMPT expression increasing the pool of cellular NAD+. The NAMPT inhibitor FK866 sensitized PDAC cells to the antiproliferative effects of metformin in vitro and decreased cellular NAD+ pool. Intriguingly, FK866 combined with metformin increased survival in mice bearing KP4 cells xenografts but not in mice with PANC1 xenografts. Transcriptome analysis revealed that the drug combination reactivated genes in the p53 pathway and oxidative stress providing new insights about the mechanisms leading to cancer cell death.

2023-06-01 | GSE210562 | GEO

siRNA profiling of nu/nu after GFP targeted knockdown to examine off target effects of GFP siRNA

Project description:siRNA mediated gene knockdown has been shown to be extremely sequence specific. However, off-target gene regulation due to partial sequence homology has also been reported. Furthermore, sequence unrelated effects on gene regulation can occur when siRNA is applied in vivo. In this experiment we investigated off target gene regulation due to treatment of mice with siRNA and LNA modified siRNA targeting GFP. Off target gene regulation was observed and was markedly reduced upon introduction of LNA modifiecation in siRNA. Experiment Overall Design: NMRI nu/nu mice were treated with saline (control), siRNA or siLNA for three weeks. Then the mice were sacrificed and tumor total RNA was isolated. The effect of siRNA/siLNA treatment was evaluated by comparing gene expression of saline treated animals with that of siRNA and siLNA treated animals respectively.

2008-06-14 | E-GEOD-6406 | biostudies-arrayexpress

Radiation response in xenografts of the head and neck cancer UT14 cell line

Project description:Low passage head and neck squamous cancer cells (UT-14-SCC) were injected into the flanks of female nu/nu mice to generate xenografts. After tumors reached a size of 500mm3, they were treated with either sham RT or 15 Gy in one fraction. At different time points, days 0, 3, 10 and for controls and days 4, 7, 12, and 21 after irradiation, the tumors were harvested for global gene expression analysis and pathway analysis.

2014-09-19 | GSE61573 | GEO

Lactobacillus phage Lc-Nu

Project description:Lactobacillus phage Lc-Nu overview

| PRJNA69581 | ENA