Calcipotriol vs. calcitriol in hepatocellular gene expression
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ABSTRACT:
PROVIDER: PRJNA415972 | ENA |
REPOSITORIES: ENA
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Project description:We aimed to explore the potential and mechanism of calcipotriol to regulate the hepatocellular transcriptome in comparison to calcitriol.
2018-06-14 | GSE106234 | GEO
Project description:Using pangenomic cDNA microarrays and qPCR techniques, we identified the genes regulated by calcitriol (1,25 (OH)D3, 10 nM) in dorsal root ganglia and/or Schwann cells. After 24 hours of calcitriol supplementation, we found a modified expression of many genes involved in axogenesis and myelination.
2012-04-07 | E-MEXP-3491 | biostudies-arrayexpress
Project description:Background: Breast cancer patients present lower 1,25(OH)2D3 or 25(OH)D3 serum levels than unaffected women. Although 1,25(OH)2D3 pharmacological concentrations of 1,25(OH)2D3 may exert antiproliferative effects in breast cancer cell lines, much uncertainty remains about the effects of calcitriol supplementation in tumor specimens in vivo. We have evaluated tumor dimension (ultrassonography), proliferative index (Ki67 expression), 25(OH)D3 serum concentration and gene expression profile, before and after a short term calcitriol supplementation (dose to prevent osteoporosis) to post-menopausal patients. Results: Thirty three patients with operable disease had tumor samples evaluated. Most of them (87.5%) presented 25(OH)D3 insufficiency (<30 ng/mL). Median period of calcitriol supplementation was 30 days. Although tumor dimension did not vary, Ki67 immunoexpression decreased after supplementation. Transcriptional analysis of 15 matched pre/post-supplementation samples using U133 Plus 2.0 GeneChip (Affymetrix) revealed 18 genes over-expressed in post-supplementation tumors. As a technical validation procedure, expression of four genes was also determined by RT-qPCR and a direct correlation was observed between both methods (microarray vs PCR). To further explore the effects of near physiological concentrations of calcitriol on breast cancer samples, an ex vivo model of fresh tumor slices was utilized. Tumor samples from another 12 post-menopausal patients were sliced and treated in vitro with slightly high concentrations of calcitriol (0.5nM), that can be attained in vivo, for 24 hours In this model, expression of PBEF1, EGR1, ATF3, FOS and RGS1 was not induced after a short exposure to calcitriol. Conclusions: In our work, most post-menopausal breast cancer patients presented at least 25(OH)D3 insufficiency. In these patients, a short period of calcitriol supplementation may prevent tumor growth and reduce Ki67 expression, probably associated with discrete transcriptional changes. This observation deserves further investigation to better clarify calcitriol effects in tumor behavior under physiological conditions.
2012-02-18 | GSE35925 | GEO
Project description:Hepatocellular carcinoma Huh7: siHINT1 vs. siControl
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Project description:Background: Breast cancer patients present lower 1,25(OH)2D3 or 25(OH)D3 serum levels than unaffected women. Although 1,25(OH)2D3 pharmacological concentrations of 1,25(OH)2D3 may exert antiproliferative effects in breast cancer cell lines, much uncertainty remains about the effects of calcitriol supplementation in tumor specimens in vivo. We have evaluated tumor dimension (ultrassonography), proliferative index (Ki67 expression), 25(OH)D3 serum concentration and gene expression profile, before and after a short term calcitriol supplementation (dose to prevent osteoporosis) to post-menopausal patients. Results: Thirty three patients with operable disease had tumor samples evaluated. Most of them (87.5%) presented 25(OH)D3 insufficiency (<30 ng/mL). Median period of calcitriol supplementation was 30 days. Although tumor dimension did not vary, Ki67 immunoexpression decreased after supplementation. Transcriptional analysis of 15 matched pre/post-supplementation samples using U133 Plus 2.0 GeneChip (Affymetrix) revealed 18 genes over-expressed in post-supplementation tumors. As a technical validation procedure, expression of four genes was also determined by RT-qPCR and a direct correlation was observed between both methods (microarray vs PCR). To further explore the effects of near physiological concentrations of calcitriol on breast cancer samples, an ex vivo model of fresh tumor slices was utilized. Tumor samples from another 12 post-menopausal patients were sliced and treated in vitro with slightly high concentrations of calcitriol (0.5nM), that can be attained in vivo, for 24 hours In this model, expression of PBEF1, EGR1, ATF3, FOS and RGS1 was not induced after a short exposure to calcitriol. Conclusions: In our work, most post-menopausal breast cancer patients presented at least 25(OH)D3 insufficiency. In these patients, a short period of calcitriol supplementation may prevent tumor growth and reduce Ki67 expression, probably associated with discrete transcriptional changes. This observation deserves further investigation to better clarify calcitriol effects in tumor behavior under physiological conditions. Post-menopausal patients with early stage breast cancer, in the absence of distant metastasis, were invited to take part in the study. This protocol was approved by the Institutional Ethics Committee, and a written informed consent was signed by all participants. Patients had blood and tumor samples collected during biopsy, and were prescribed calcitriol supplementation, (Rocaltrol)TM 0.50 g/day PO, as recommended for osteoporosis prevention. Tumor specimens obtained during biopsy (pre-supplementation) or breast surgery (post-supplementation) were hand dissected and samples with at least 70% tumor cells were further processed. Breast surgery followed in about one month
2012-02-18 | E-GEOD-35925 | biostudies-arrayexpress
Project description:Effects of calcitriol on expressions of ER stress related genes were evaluated with microarray. Calcitriol, the active form of vitamin D, is known to induce apoptosis in cancer cells and increase intracellular calcium. Increase in cytopalsmic calcicium levels may indicate a decrease in endoplasmic reticulum (ER) calcium levels since ER is the main storage unit for calcium. Decrease in ER calcium levels are known to induce ER stress which can lead to apoptosis. However the effects of calcitriol on ER stress have not been reported before. Here we hypotesized that the cellular effects of calcitriol can be explained by induction of ER stress. We have tested this hypothesis by assessing calcitriol induced transcriptomic alterations with a focus on ER stress related genes.
2015-01-01 | GSE53975 | GEO
Project description:Dicer is a key endoribonuclease of the microRNA biogenetic machinery. Downregulation of Dicer has been associated with aberrant expression of microRNAs and the promotion of tumorigenesis. Calcitriol, the hormonal form of vitamin D3, increases microRNA expression in tumor cells, but the mechanism is not yet understood. Given the essential role of Dicer in microRNAs biogenesis, the purpose of this study was to evaluate whether this gene is a target for calcitriol and to explore the effects of this hormone on microRNA expression. Our findings demonstrate that calcitriol increased Dicer mRNA and protein in SiHa and HeLa cervical cancer cells, which expressed the vitamin D receptor. The inductive effect of calcitriol on Dicer mRNA was not observed in C33-A cells lacking this nuclear receptor. To explore the potential effect of Dicer upregulation by calcitriol on microRNA processing, we performed a microRNA profiling study in SiHa cells treated with calcitriol. The analysis of microRNA expression revealed that this hormone promotes the maturation of a subset of microRNAs with potential regulatory function in cancer pathways. Among these, miR-22 and miR-296-3p have already been associated with tumor-supressive effects. Our results suggest that Dicer upregulation by calcitriol could be associated, at least in part, with an increase in the maturation of a subset of tumor-suppressor microRNAs in cervical cancer cells.
2014-11-30 | GSE61829 | GEO
Project description:The mechanism of action of vitamin D in prostate cancer (PCa) remains poorly defined, with most mechanisms identified being highly cell type and model specific. One of the underlying factors for these diverse mechanisms may be the use of overly simplistic in vitro model systems to study the complex biology of vitamin D response. Here we use the more complex and in vivo transgenic adenocarcinoma of mouse prostate (TRAMP) model to better determine the mechanism by which vitamin D inhibits PCa growth. In these studies early stage TRAMP mice were treated M-BM-1 20M-NM-<g/kg calcitriol (vitamin D) on a Monday/Wednesday/Friday schedule and tissue was procured 12 and 24 hours post treatment to assess changes in PCa transcriptomes using Affymetrix gene expression arrays. 15 total samples were analyzed. 10 week old TRAMP mice were treated IP M-BM-1 20 ug/kg calcitriol on a Monday/Wednesday/Friday (MWF) schedule, and prostate tissue was procured 12 (N=3, control; N=4, calcitriol) and 24 hours (N=4, control; N=4, calcitriol) post treatment for use in affymetrix studies.
2015-03-02 | E-GEOD-57382 | biostudies-arrayexpress
Project description:Glioblastoma is the most common primary brain cancer and is associated with poor survival and high rates of recurrent diseases. The median survival using standard radio-chemotherapy is 15 months and the 5-year survival rate is below 5%. It is hypothesized that treatment resistance, diffuse infiltration of the brain and disease recurrence is, at least in part, due to cancer cells that can obtain a transient, stem-like phenotype. These so-called glioma stem-like cells (GSCs) display pluripotency, express marker proteins associated with stem-cells and can replenish the tumor after treatment. Recently, we have shown that the hormonally active form of vitamin D3, calcitriol (1α,25(OH)2-vitamin D3), is active in a subset of GSCs and reduces traits of stemness. Here, we have employed a set of 8 GSCs that do not respond to calcitriol-treatment (No-responder) and the 8 strongest responders to calcitriol (High-responder) and compared to proteomes after treatment with 50 nM calcitriol for 48h.
2023-11-04 | PXD041634 | Pride
Project description:Transcriptional profiling of hepatocellular carcinoma vs. matched noncancerous liver tissue
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