Calcipotriol vs. calcitriol in hepatocellular gene expression
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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.
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Project description:We investigated how Am80 differed from vitamin D analogues in terms of effects on gene expression in PDAC CAFs. we stimulated primary cultured PSCs isolated from three patients with PDAC (PSC163, PSC52, and PSC119) with dimethyl sulfoxide (DMSO, control), Am80, or calcipotriol. Gene expression profiles were then compared using microarray-based transcriptomic analysis. Extracting genes that were differentially expressed between Am80- and calcipotriol-treated cells revealed that Meflin expression was more significantly upregulated by Am80 than calcipotriol. Interestingly, the expression levels of fibroblast activation protein (FAP) and chemokine (C-C motif) ligand 2 (CCL2), which are markers of pCAFs, were higher in Am80-treated PSCs than calcipotriol-treated PSCs, whereas the expression levels of other pCAF marker genes, such as C-X-C motif chemokine ligand 12 (CXCL12), podoplanin (PDPN) and periostin (POSTN), were higher in calcipotriol-treated cells. These data suggested that Am80 and calcipotriol differentially regulated gene expression in PSCs.
2021-07-03 | GSE179318 | GEO
Project description:Further investigation is needed to understand the role of vitamin D in muscle function. In this study, we utilized SOD1 gene knockout mice as a model of muscular atrophy and intervened with the VDR ligand calcipotriol to observe its effects on muscle function. RNAseq analysis was employed to examine the impact of calcipotriol on gene expression in the gastrocnemius muscle, aiming to elucidate its underlying mechanisms. The results revealed that calcipotriol primarily exerted its effects through pathways related to protein synthesis and mitochondrial function.
2024-12-01 | GSE249868 | GEO
Project description:To investigate the effect of calcipotriol treatment, chaetocin treatment and VDR knockdown on gene expression primary normal human fibroblasts, we treated BJ cells with 100 nM calcipotriol for 4 or 24 hours, 50 nM chaetocin for 24 hours, knocked down VDR with si RNA respectively. Then, we performed RNA-seq analysis.
2023-02-11 | GSE224311 | GEO
Project description:To find which signaling affects the therapy of calcipotriol in breast cancer therapy
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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
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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.
2012-02-18 | GSE35925 | GEO
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