Expression profile of human HepG2 cells treated with PADMA28 ethanolic extracts or EtOH solvent control
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ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Oliver Wrulich
PROVIDER: E-GEOD-40580 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:The aim of this study was to analyze the influence of PADMA28 ethanolic extracts on HepG2 gene expression. PADMA28 (Swissmedic Nr. 58436) is an Indo-Tibetan polyherbal preparation used for the treatment of symptoms associated with circulatory disorders.
2012-10-01 | GSE40580 | GEO
Project description:Growth factor signaling and angiogenesis may promote endocrine-resistance in breast cancer and blocking these pathways can overcome resistance in preclinical models. We conducted a phase-II study of adding the VEGFR/Ras/Raf/MAPK inhibitor sorafenib to endocrine therapy in metastatic ER-positive breast cancer, either upon progression or after maximal response with measurable residual disease. Tumor biopsies and serum were collected on days 1 and 28. Primary endpoint was response by RECIST after 3 months and secondary endpoints included safety, time to progression (TTP), and biomarker assessment. Planned sample size was 43 patients but the study closed after 11 patients because of slow accrual. 8 patients had progressive disease (PD) on entry and 3 had stable disease (SD). One patient with SD discontinued sorafenib after 2-weeks because of grade 3 rash. Of the 10 remaining patients after adding sorafenib, 7 had SD (70%), 3 had PD (30%) and median TTP was 6.1-months. Of the 8 patients who entered the study with PD on endocrine therapy, 5 converted to SD (62%) with a median TTP of 6.4-months. Notably, patients on tamoxifen had a median TTP of 8.4-months. The most common adverse events were hypophosphatemia, hypokalemia, and rash, and the majority were grade 1&2 with no grade 4 toxicities. There was a significant reduction in serum VEGFR2 and PDGFR-α on day-28 (p-values 0.0035 and 0.017, respectively). Both serum VEGF and sVEGFR-1 were increased on day-28, but the differences were not statistically significant (p-values 0.3223 and 0.084, respectively). Microarray analysis identified 32 suppressed genes with an FDR of <0.20 and at least a 2-fold change with no induced genes and 29 KEGG pathways were enriched on day-28. Our study suggests that sorafenib can restore endocrine sensitivity, particularly tamoxifen, and this strategy of adding novel agents in patients progressing on endocrine therapy should be examined in future trials. This was a single-institution, phase II study of adding sorafenib to existing endocrine therapy. On study entry, eligible patients underwent serum sample collection and core biopsy of accessible disease (if applicable) on endocrine therapy and prior to starting sorafenib. Serum and a second biopsy were then collected on day 28. Sorafenib dose was 400mg orally twice daily along with continuing the same endocrine agent. Patients were followed monthly for clinical and toxicity evaluation. Disease response by RECIST criteria was assessed after 3 months by appropriate scans and these were obtained every 2 months thereafter until progression. Sorafenib and the endocrine agent were continued until disease progression or unacceptable toxicity
2012-09-13 | E-GEOD-40837 | biostudies-arrayexpress
Project description:Introduction: The Epithelial Cell Adhesion Molecule (EpCAM) has been shown to be strongly expressed in human breast cancer and cancer stem cells and its overexpression has been supposed to support tumor progression and metastasis. However, effects of EpCAM overexpression on normal breast epithelial cells have never been studied before. Therefore, we analyzed effects of transient adenoviral overexpression of EpCAM on proliferation, migration and differentiation of primary human mammary epithelial cells (HMECs). METHODS: HMECs were transfected by an adenoviral system for transient overexpression of EpCAM. Thereafter, changes in cell proliferation and migration were studied using a real time measurement system. Target gene expression was evaluated by transcriptome analysis in proliferating and polarized HMEC cultures. A Chicken Chorioallantoic Membrane (CAM) xenograft model was used to study effects on in vivo growth of HMECs. RESULTS: EpCAM overexpression in HMECs did not significantly alter gene expression profile of proliferating or growth arrested cells. Proliferating HMECs displayed predominantly glycosylated EpCAM isoforms and were inhibited in cell proliferation and migration by upregulation of p27KIP1 and p53. HMECs with overexpression of EpCAM showed a down regulation of E-cadherin. Moreover, cells were more resistant to TGF-beta1 induced growth arrest and maintained longer capacities to proliferate in vitro. EpCAM overexpressing HMECs xenografts in chicken embryos showed hyperplastic growth, lack of lumen formation and increased infiltrates of the chicken leukocytes. CONCLUSIONS: EpCAM revealed oncogenic features in normal human breast cells by, inducing resistance to TGF-beta1-mediated growth arrest and supporting a cell phenotype with longer proliferative capacities in vitro. EpCAM overexpression resulted in hyperplastic growth in vivo. Thus, we suggest that EpCAM acts as a prosurvival factor counteracting terminal differentiation processes in normal mammary glands. Differential expression was assessed with the moderated t-test (Bioconductor's limma package) with pairing of the samples by the donor. Raw p-values were adjusted for multiple hypothesis testing using the method from Benjamini and Hochberg for a strong control of the false discovery rate. EPCAM and GFP over-expression in proliferating mammary epithelial cells from two donors (6 and 8). Expression levels between EPCAM and control samples were compared to determine whether, and to which extent EPCAM over-expression alters the gene expression profile of the cells.
2013-06-13 | E-GEOD-39071 | biostudies-arrayexpress
Project description:The eukaryotic translation initiation factor (eIF) 3a is described in various tumor entities as potential tumor marker involved in development and progression of cancer. eIF3a is the largest subunit of the eIF3 complex, a key functional entity in 80S establishment and translation initiation. We hypothesize that eIF3a is more a specific than global translation initiator and involved in signalling pathways that are frequently targeted in UBC therapy. Methods: In FFPE samples of UBC patients eIF3a expression was analysed together with overall survival. In cell culture we investigated proliferation, migration, clonogenicity and tumorgenicity of UBC cell lines with and without knockdown of eIF3a and compared the cytotoxicity of eIF3a knockdown with other translational inhibitors, including the chemotherapeutic Rapamycine. Detailed information on changed gene expression and global translation initiation were gathered by mRNA expresssion and polysomal profiling. Results: and Conclusion eIF3a is upregulated in UBC and high expression of eIF3a corresponds with longer overall survival in low grade tumors. Knockdown of eIF3a in UBC cell lines reduces their malignant phenotype, including reduced tumor growth in xenotransplanted mice. eIF3a regulates DNA damage response (ATM, ATR, CDC25A) on a translational level and we show that reduction in eIF3a expression does not hamper global translation initiation. The knockdown of eIF3a strongly influences proliferation of UBC cell lines without dramatically disturbing general translation as depicted in polysomal profiles. We therefore analysed potential changes on the mRNA level in eIF3a knockdown compared to control HT1197 cells. Differential expression of genes between eIF3a knock-down and control samples was assessed with the moderated t-test (Bioconductor's limma package). Raw p-values were adjusted for multiple hypothesis testing using the method from Benjamini and Hochberg for a strong control of the false discovery rate.
2014-08-12 | E-GEOD-45636 | biostudies-arrayexpress
Project description:We identified directly and indirectly regulated target genes utilizing an inducible TEL-AML1 system derived from the murine pro B-cell line BA/F3 and a monoclonal antibody directed against TEL-AML1. By integration of promoter binding identified with ChIP-on-chip, gene expression and protein output through microarray technology and stable labelling of amino acids in cell culture (SILAC), we identified directly and indirectly regulated targets of the TEL-AML1 fusion protein. Bound promoter regions of immunoprecipitated TEL-AML1 associated genes were first compared to input material and enrichment was calculated. The same was performed for empty vector control cell lines, also treated with the induction reagent mifepriston. Enriched promoter regions were then compared of the both sets. 2 independent replicates each (4 arrays) were performed.
2013-11-04 | E-GEOD-50735 | biostudies-arrayexpress
Project description:Evaluation of the effect of ABL2 knockdown in HepG2 cells following treatment with alcohol
2023-10-03 | GSE218773 | GEO
Project description:The transcriptomics changes induced in the human liver cell line HepG2 by Cyclosporin A after treatment for 12h, 24h, 48h and 72h The study investigated differential gene expression in HepG2 cell line mRNA following 12, 24, 48 and 72 hours of exposure to Cyclosporin A and solvent. Three biological replicates per compound/solvent. In total 36 arrays.
2015-01-27 | E-GEOD-45635 | biostudies-arrayexpress
Project description:The transcriptomics changes induced in the human liver cell line HepG2 by 17 hepatotoxic compounds, 5 non-hepatotoxic compounds and solvent controls after treatment for 24h The study investigated differential gene expression in HepG2 cell line mRNA following 24 hours of exposure to 17 hepatotoxic compounds, 5 non-hepatotoxic compounds and solvent controls. Three biological replicates per compound/solvent. In total 105 arrays .
2014-02-14 | E-GEOD-51952 | biostudies-arrayexpress
Project description:The microRNA changes induced in the human liver cell line HepG2 by Cyclosporin A after treatment for 12h, 24h, 48h and 72h The study investigated differential microRNA expression in HepG2 cell line following 12, 24, 48 and 72 hours of exposure to Cyclosporin A and solvent. Three biological replicates per compound/solvent. In total 36 arrays .
2015-01-27 | E-GEOD-45800 | biostudies-arrayexpress
Project description:The transcriptomics changes induced in the human liver cell line HepG2 by low and high doses of acetaminophen and solvent controls after treatment for 4 time points (12h, 24h, 48h and 72h) The study investigated differential gene expression in HepG2 cell line mRNA following 12 to 72 hours of exposure to low and high doses of acetaminophen and solvent controls. Three biological replicates per compound/solvent.
2015-12-15 | E-GEOD-53216 | biostudies-arrayexpress