Expression data from PC3 cells treated with astragalus polysaccharides
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PROVIDER: PRJNA565721 | ENA |
REPOSITORIES: ENA
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Project description:Astragalus polysaccharides (APS), as one of the main effective components of astragalus, have been reported to regulate the processes of inflammation, metabolism, and carcinogenes. We used microarrays to detect the different expression of mRNA in PC3 cells upon APS treatment.
2019-09-17 | GSE137486 | GEO
Project description:To identify biomarkers regulated by traditional Chinese medicine Astragalus membranaceus Fischer Bge. var. mongolicus Bge. Hsiao in colorectal cancer. We have identified several differentially expressed genes including microRNAs using Affymetrix HTA-2.0 array. In this dataset, we include the expression data obtained from colon cancer cell line HCT116 grafted into nude mice. The mice was treated either water or traditional Chinese medicine Astragalus membranaceus for 28 days. These data are used to obtain 1425 genes that are differentially expressed in response to Astragalus membranaceus treatment.
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Project description:Objective: To study the effect of astragalus polysaccharide combined with metformin on mRNA expression profile of type 2 diabetic mice, and to explore the molecular mechanism of astragalus polysaccharide combined with metformin in the treatment of type 2 aging diabetes. Methods: Natural aging mice were induced by high-sugar and high-fat diet combined with streptozotocin to prepare aging diabetes model. The experimental mice were divided into aging control group, aging diabetes model group, metformin treatment group, astragalus polysaccharide and metformin. The treatment group was treated with gavage for 60 consecutive days. Immunohistochemical detection of insulin levels in pancreatic tissue of each group of mice, serum insulin levels were measured by mouse insulin kit to observe the treatment of aging diabetes and astragalus polysaccharide combined with metformin; using Agilent mouse whole gene expression profile chip The mRNA expression changes of liver tissues in each group were analyzed, and the differential genes were screened by bioinformatics tools and the differential genes and signal pathways were enriched and analyzed. Results: Compared with the aging group, the insulin and insulin antibody levels in the model group were significantly decreased (P<0.05). Compared with the model group, the insulin and insulin antibody levels in the two treatment groups increased (P<0.05), and jaundice The level of polysaccharide in combination with metformin was significantly higher than that in metformin group (P<0.05). The differential gene analysis of the chip showed that there were 5617 differential genes in the aging diabetes model group, 3131 were up-regulated, and 2486 were down-regulated; the Astragalus polysaccharide combined with metformin treatment group had 4767 differential genes, compared with the aging diabetes model group. 2143 up-regulated, 2624 down-regulated, genes with significant differences were mainly involved in protease activity and drug metabolism, and significantly enriched into 33 signaling pathways (P<0.01). Conclusion: The gene regulatory network plays an important role in the intervention of Astragalus polysaccharides and metformin in the treatment of aging type 2 diabetes.
2019-12-06 | GSE124813 | GEO
Project description:Objective: To study the effect of astragalus polysaccharide combined with metformin on mRNA expression profile of type 2 diabetic mice, and to explore the molecular mechanism of astragalus polysaccharide combined with metformin in the treatment of type 2 aging diabetes. Methods: Natural aging mice were induced by high-sugar and high-fat diet combined with streptozotocin to prepare aging diabetes model. The experimental mice were divided into aging control group, aging diabetes model group, metformin treatment group, astragalus polysaccharide and metformin. The treatment group was treated with gavage for 60 consecutive days. Immunohistochemical detection of insulin levels in pancreatic tissue of each group of mice, serum insulin levels were measured by mouse insulin kit to observe the treatment of aging diabetes and astragalus polysaccharide combined with metformin; using Agilent mouse whole gene expression profile chip The mRNA expression changes of liver tissues in each group were analyzed, and the differential genes were screened by bioinformatics tools and the differential genes and signal pathways were enriched and analyzed. Results: Compared with the aging group, the insulin and insulin antibody levels in the model group were significantly decreased (P<0.05). Compared with the model group, the insulin and insulin antibody levels in the two treatment groups increased (P<0.05), and jaundice The level of polysaccharide in combination with metformin was significantly higher than that in metformin group (P<0.05). The differential gene analysis of the chip showed that there were 5617 differential genes in the aging diabetes model group, 3131 were up-regulated, and 2486 were down-regulated; the Astragalus polysaccharide combined with metformin treatment group had 4767 differential genes, compared with the aging diabetes model group. 2143 up-regulated, 2624 down-regulated, genes with significant differences were mainly involved in protease activity and drug metabolism, and significantly enriched into 33 signaling pathways (P<0.01). Conclusion: The gene regulatory network plays an important role in the intervention of Astragalus polysaccharides and metformin in the treatment of aging type 2 diabetes.
2022-06-12 | GSE132599 | GEO
Project description:On the basis of the clear role of Astraglus polysaccharides (APS) in the prevention of obesity and non-alcoholic fatty liver (NAFLD) induced by high-fat diet, the potential effector genes of APS are screened by means of transcriptional techniques.
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Project description:SD rats were intramuscular injected with dexamethasone to induce osteoporosis, and treated with APS. Then, colonic epithelia of control, osteoporotic and APS-treated osteoporotic rats were collected for MethylC-capture sequencing .
2023-08-03 | GSE155589 | GEO
Project description:We conduct transcriptome comparison of control and WHSC1 depleted PC3 cells to gain genomic insights on the biological processes that WHSC1 is involved in prostate cancer cells. More than 2000 known genes were found changed in the WHSC1 depleted cells. Ingenuity Pathway Analysis (IPA) and Gene Set Enrichment Analysis (GSEA) show that the most prominent altered pathways in the WHSC1 depleted cells are related to regulation of actin-based motility, mTOR signaling pathway.
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Project description:Transcriptional profiles were examined in PC3 prostate cancer cells treated with vehicle (DMSO), vorinostat (VOR, HDACi), GSK126 (GSK126, EZH2i) or all 3 agents (COMBO) at 72 hours, prior to the commencement of cell death, to investigate the molecular mechamism by which these drugs and their combinations are functioning.
2020-05-05 | GSE149784 | GEO
Project description:Inhibitors of Wnt signaling have been previously shown to be involved in prostate cancer (PC) metastasis; however the role of Sclerostin (Sost) has not yet been explored. Here we show that elevated Wnt signaling derived from Sost deficient osteoblasts (OBSOSTKO) promotes PC invasion while rhSOST has an inhibitory effect. In contrast, rhDKK1 promotes PC elongation and filopodia formation, morphological changes characteristic of an invasive phenotype. Furthermore, rhDKK1 was found to activate canonical Wnt signaling in PC3 cells as quantified by TOPFLASH reporter and b-catenin activity, suggesting that SOST and DKK1 have opposing roles on Wnt signaling in this context. Gene expression analysis of PC3 cells co-cultured with OBs exhibiting varying amounts of Wnt signaling identified CRIM1 as one of the transcripts up-regulated under highly invasive conditions. Following further analysis we found that CRIM1 increases PC3 invasion, complexes with b-catenin, and promotes cell-adhesion, suggesting that elevated Wnt signaling secreted from the bone may promote PC tropism by promoting CRIM1 expression and facilitating cancer cell invasion and adhesion to bone. We concluded that SOST and DKK1 have opposing effects on PC3 cell invasion and that bone-derived Wnt signaling positively contributes to the invasive phenotypes of metastatic cancer cells by activating CRIM1 expression and facilitating PC-OB physical interaction. As such, we investigated the effects of high concentrations of SOST in vivo. We found that PC3-cells overexpressing SOST injected via tail vein did not readily metastasize in NSG xenografts, suggesting that targeting the molecular bone environment may influence bone metastatic outcome in clinical settings.
2014-04-08 | GSE56582 | GEO