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Anti-cnacer effects of ginsenoside Rh2 with doxorubicin from breast tumor bearing mice

ABSTRACT: Anti-cnacer effects of ginsenoside Rh2 with doxorubicin from breast tumor bearing mice

PROVIDER: PRJNA774507 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16573711_1.fastq.gz	Fastqsanger.gz
	SRR16573711_2.fastq.gz	Fastqsanger.gz
	SRR16573712_1.fastq.gz	Fastqsanger.gz
	SRR16573712_2.fastq.gz	Fastqsanger.gz
	SRR16573713_1.fastq.gz	Fastqsanger.gz

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Anti-cnacer effects of ginsenoside Rh2 with doxorubicin from breast tumor bearing mice

Project description:The FDA approved drug Doxorubicin provokes copious irreversible cardiotoxicity and even increases the risk of heart failure. Considering the multiple and interacted molecular pathways in cancer, there is a big possibility that tumors are simultaneously sensitive to different drugs. This makes achievable to study the combinations of drug, having the virtues of less toxicity, higher efficacy and potentially antagonizing drug resistance in cancer therapy. In the present study, we addressed the synergistic effects of ginsenoside Rh2 on doxorubicin-treated breast cancer bearing mice. We showed that Rh2 significantly enhanced the anti-cancer effects of doxorubicin and greatly attenuated the cardiotoxicity. Transcriptomic changes can clearly distinguish the chemotherapeutic groups and non-treated control groups. Transcriptomic analysis domestrated that Rh2 protection involved in multiple vital pathways including cellular stress, apoptosis and inflammation.

2021-10-28 | GSE186555 | GEO

Protective effects of ginsenoside Rh2 on doxorubicin damaged hearts from breast tumor bearing mice

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Protective effects of ginsenoside Rh2 on doxorubicin damaged hearts from breast tumor bearing mice

Project description:Protective effects of ginsenoside Rh2 on doxorubicin damaged hearts from breast tumor bearing mice

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Project description:The breast cancer incidence has been increasing in China, with the earlier age of onset compared with Western countries. Traditional Chinese medicine has been provided as one of the major source of anti-cancer drugs. Ginseng is one of the most common traditional medicines in China. Ginsenosides, the saponins in the plant Panax (ginseng) are the major active components responsible for their chemopreventive effects from cancer. However, the mechanisms by which ginsenosides exert their anti-cancer effect remain elusive. By combining TMT-based quantitation with TiO2-based phosphopeptide enrichment, we performed a quantitative analysis of the changes of the phosphoproteomes in ginsenoside Rg3-treated breast cancer MDA-MB-231 cells. We were able to quantitate 5,140 phosphorylation sites on 2,041 phosphoproteins. Our data show that the phosphorylation status of 13 sites was changed in MDA-MB-231 cells upon Rg3 treatment. The perturbed phosphoproteins are CPSF7, EEF2, HIRIP3, MAGED2, MPRIP, MYCBP2, PAWR, PPP1R12A, RANBP2, SEPT9, TMPO, and UFL1. These proteins are involved in various biological processes, including protein synthesis, cell division, and inhibition of NF-κB signaling. Our study revealed that Rg3 exerts its anti-cancer effects through a combination of different signaling pathways.

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Project description:The angio-suppressive effect of 20(R)-ginsenoside Rg3 (Rg3-R) has been previously demonstrated, and microRNAs (miRNAs) are a vital group of small non-coding RNAs that function as post-transcriptional modulator of gene expression. Thus, using human umbilical vein endothelial cells (HUVEC) as model, we compared the microRNA (miRNA) expression profile of vascular endothelial growth factor (VEGF)-induced cells with the profile of the cell co-treated with VEGF and Rg3-R. Among the screened 553 human miRNAs, 6 up-regulated (miR-520h, miR-487b, miR-197, miR-524*, miR-342 and miR-219) and 3 down-regulated (miR-23a, miR-489 and miR-377) miRNAs were detected in Rg3-R treated vascular endothelial growth factor (VEGF)-induced HUVECs compared to VEGF alone. Real time RT-PCR was subsequently performed to verify the miRNA microarray result. Two condition experiment: VEGF-induced HUVEC and VEGF-induced HUVEC treated with Rg3-R. Three independent microarray experiments, with triplicate per microarray.

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