Calcitriol-Driven IL-10 IL-22 ILC Differentiation from ILCPs
Ontology highlight
ABSTRACT:
INSTRUMENT(S):
ORGANISM(S): Mus Musculus (mouse)
TISSUE(S): Bone Marrow
SUBMITTER: 
Qingyang Liu
LAB HEAD: Qingyang Liu
PROVIDER: PXD068530 | Pride | 2026-07-14
REPOSITORIES: Pride
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Project description:Vitamin D deficiency is associated with a decline in muscle function and an increasing risk of muscle injury in athletes and the elderly. Nevertheless, how vitamin D3 and vitamin D receptor (VDR) regulate skeletal muscle cells under pro-fibrotic factor stimulation that could be pronounced during repetitive muscle damage have not been elucidated. Therefore, this study aimed to investigate the regulatory role of cholecalciferol (D3), calcidiol (25D3), calcitriol (1,25D3), and the effect of Vdr gene suppression under TGF-β1 stimulation in C2C12 mouse skeletal muscle cells. All forms of vitamin D3 exerted anti-fibrotic effects under TGF-β1 stimulation by suppression of COL1A1; however, D3 preserves this effect without a negative impact on myogenesis. Moreover, LC-MS/MS-based proteomics analysis revealed that myoblast fusion protein and mitochondrial regulation were altered following Vdr knockdown. These changes were associated with exacerbation of α-SMA expression in TGF-β1-treated cells and suggested VDR modulates fibrogenesis in skeletal muscle cells regardless of ligand binding. Under TGF-β1 stimulation, anti-fibrotic effects of 1,25D3 but not D3 were diminished after Vdr knockdown, supporting D3 action is not dependent on VDR activation. Collectively, understanding anti-fibrotic effects of vitamin D3 is beneficial for providing a strategy of vitamin D supplementation to counteract fibrosis development after muscle injury.
2025-12-01 | PXD062669 | Pride
Project description:Vitamin D induces anti-proliferative and differentiating effects in prostate cancer. Thus calcitriol, the hormonally active form of Vitamin D, and its analogs have been extensively studied in prostate cancer cells. Yet despite its importance, relatively little is known about the genome-scale mechanisms by which Vitamin D, through its cognate nuclear vitamin D receptor (VDR), exerts its regulatory functions at the genomic level. In this study, we defined VDR transcriptional networks in the LNCaP prostate cancer cell line by mapping the genomic binding sites of VDR and by identifying differentially expressed genes upon calcitriol treatment. We found that VDR and androgen receptor (AR) antagonistically regulate a subset of cell cycle-related genes that are over-expressed in prostate cancer tumors. The expression balance of these genes is partially regulated through the competition dynamics between AR and VDR binding to shared cis-regulatory elements. On such shared elements, we found that FOXA1 mediates this competition by serving as a pioneering factor for both AR and VDR binding. We also found significant enrichment of AR-, VDR-, and AR/VDR overlapping binding sites in prostate cancer-associated single-nucleotide polymorphism (SNP) intervals identified from genome-wide association studies (GWAS), providing genetic evidence to link AR, VDR and their crosstalk to prostate cancer susceptibilities. In particular, we found that in a cis-regulatory element of the RFX6 gene implicated in prostate cancer progression, an allelic variant increases prostate cancer risk by switching the antagonism between AR and VDR into a synergistic interaction. Examination of AR, VDR, and FOXA1 binding in LNCaP cells, in biological replicates
2015-08-01 | E-GEOD-64656 | biostudies-arrayexpress
Project description:Vitamin D induces anti-proliferative and differentiating effects in prostate cancer. Thus calcitriol, the hormonally active form of Vitamin D, and its analogs have been extensively studied in prostate cancer cells. Yet despite its importance, relatively little is known about the genome-scale mechanisms by which Vitamin D, through its cognate nuclear vitamin D receptor (VDR), exerts its regulatory functions at the genomic level. In this study, we defined VDR transcriptional networks in the LNCaP prostate cancer cell line by mapping the genomic binding sites of VDR and by identifying differentially expressed genes upon calcitriol treatment. We found that VDR and androgen receptor (AR) antagonistically regulate a subset of cell cycle-related genes that are over-expressed in prostate cancer tumors. The expression balance of these genes is partially regulated through the competition dynamics between AR and VDR binding to shared cis-regulatory elements. On such shared elements, we found that FOXA1 mediates this competition by serving as a pioneering factor for both AR and VDR binding. We also found significant enrichment of AR-, VDR-, and AR/VDR overlapping binding sites in prostate cancer-associated single-nucleotide polymorphism (SNP) intervals identified from genome-wide association studies (GWAS), providing genetic evidence to link AR, VDR and their crosstalk to prostate cancer susceptibilities. In particular, we found that in a cis-regulatory element of the RFX6 gene implicated in prostate cancer progression, an allelic variant increases prostate cancer risk by switching the antagonism between AR and VDR into a synergistic interaction. Gene expression profiling in LNCaP cells after 24hr treatment with different nuclear recpetor ligrands, with time-matching control, in triplicates Expression is assayed with Agilent G4112F.
2015-08-01 | E-GEOD-60956 | biostudies-arrayexpress
Project description:The vitamin D endocrine system, primarily mediated by its principal metabolite calcitriol and the vitamin D receptor (VDR), plays a critical role in numerous physiological processes in humans, ranging from calcium metabolism to the prevention of various tumors, including cervical cancer. To comprehensively understand the genomic regulatory effects of calcitriol in a cervical cancer model, this study investigated the transcriptional changes induced by calcitriol in CaSki cells, a cervical cell line harboring multiple copies of HPV16, the primary causal agent of cervical cancer. Initially, we characterized the presence and functionality of the VDR and its co-receptor retinoid X receptor in CaSki cells via immunofluorescence. Subsequently, we assessed the global transcriptome response to calcitriol treatment compared to its vehicle control using microarray analysis, with validation conducted through qPCR and western blot analysis. Our findings revealed that calcitriol regulated over 1000 protein-coding genes, along with some long non-coding RNAs and microRNAs. Overall, calcitriol exerted a repressive effect on the CaSki cell transcriptome, suppressing twice as many genes as it induced. Functional analysis of the results demonstrated that calcitriol suppressed crucial cellular processes involved in cell progression, particularly inhibiting cell proliferation, a finding validated in this study. These results suggest that in this advanced cervical cancer model, calcitriol exhibits a significant antitumor effect by blocking critical processes for tumor progression, underscoring the importance of maintaining adequate vitamin D nutritional status for cervical cancer prevention.
2025-02-25 | GSE267715 | GEO
Project description:Vitamin D induces anti-proliferative and differentiating effects in prostate cancer. Thus calcitriol, the hormonally active form of Vitamin D, and its analogs have been extensively studied in prostate cancer cells. Yet despite its importance, relatively little is known about the genome-scale mechanisms by which Vitamin D, through its cognate nuclear vitamin D receptor (VDR), exerts its regulatory functions at the genomic level. In this study, we defined VDR transcriptional networks in the LNCaP prostate cancer cell line by mapping the genomic binding sites of VDR and by identifying differentially expressed genes upon calcitriol treatment. We found that VDR and androgen receptor (AR) antagonistically regulate a subset of cell cycle-related genes that are over-expressed in prostate cancer tumors. The expression balance of these genes is partially regulated through the competition dynamics between AR and VDR binding to shared cis-regulatory elements. On such shared elements, we found that FOXA1 mediates this competition by serving as a pioneering factor for both AR and VDR binding. We also found significant enrichment of AR-, VDR-, and AR/VDR overlapping binding sites in prostate cancer-associated single-nucleotide polymorphism (SNP) intervals identified from genome-wide association studies (GWAS), providing genetic evidence to link AR, VDR and their crosstalk to prostate cancer susceptibilities. In particular, we found that in a cis-regulatory element of the RFX6 gene implicated in prostate cancer progression, an allelic variant increases prostate cancer risk by switching the antagonism between AR and VDR into a synergistic interaction.
2015-08-01 | GSE64656 | GEO
Project description:Vitamin D induces anti-proliferative and differentiating effects in prostate cancer. Thus calcitriol, the hormonally active form of Vitamin D, and its analogs have been extensively studied in prostate cancer cells. Yet despite its importance, relatively little is known about the genome-scale mechanisms by which Vitamin D, through its cognate nuclear vitamin D receptor (VDR), exerts its regulatory functions at the genomic level. In this study, we defined VDR transcriptional networks in the LNCaP prostate cancer cell line by mapping the genomic binding sites of VDR and by identifying differentially expressed genes upon calcitriol treatment. We found that VDR and androgen receptor (AR) antagonistically regulate a subset of cell cycle-related genes that are over-expressed in prostate cancer tumors. The expression balance of these genes is partially regulated through the competition dynamics between AR and VDR binding to shared cis-regulatory elements. On such shared elements, we found that FOXA1 mediates this competition by serving as a pioneering factor for both AR and VDR binding. We also found significant enrichment of AR-, VDR-, and AR/VDR overlapping binding sites in prostate cancer-associated single-nucleotide polymorphism (SNP) intervals identified from genome-wide association studies (GWAS), providing genetic evidence to link AR, VDR and their crosstalk to prostate cancer susceptibilities. In particular, we found that in a cis-regulatory element of the RFX6 gene implicated in prostate cancer progression, an allelic variant increases prostate cancer risk by switching the antagonism between AR and VDR into a synergistic interaction.
2015-08-01 | GSE60956 | GEO
Project description:Analysis of acute effects of ligand-treatment on vitamin D receptor binding genome-wide using ChIP-seq. THP-1 monocytic leucemia cells were treated with 1?,25(OH)2D3 (1,25D) or left unstimulated to investigate the acute effects of VDR chromatin occupancy. We identified in total 2340 VDR binding sites with and without the ligand. Without the ligand, there is a considerable presence of VDR already on the chromatin. However, upon a short (40 min) ligand treatment VDR shifts from sites that rarely contain a DR3 type element to sites that frequently contain one or more DR3-type element. Genome-wide identification of VDR binding in THP-1 cells at the unstimulated state and after 40 min ligand (10 nM 1?,25(OH)2D3 (1,25D, calcitriol)) treatment.
2011-08-17 | E-GEOD-27437 | biostudies-arrayexpress
Project description:Background: Vitamin D3 (VD3), a crucial fat-soluble vitamin, primarily exists in the form of calcitriol, a steroid hormone. Both exhibit anti-neoplastic activity towards several types of cancer, although the underlying mechanism is still not fully understood. Herein, we investigated the mechanism of inhibition of erytho-leukemogenesis by VD3 and calcitriol. Methods: RNAseq analysis was used to explore the effect of VD3 and calcitriol on gene expression in leukemic cells. An animal model of erythro-leukemia was used to test the effect of both compounds in vivo. CHAC1 and VDR expression was knocked-downed in leukemia cells (genotype of the samples: chac1/vdr knockdown) via lentivirus-shRNA. CHAC1 expression was overexpressed in leukemia cells (genotype of the samples: chac1 overexpression) via lentivirus-RNA. Western blotting, RT-qPCR, cell cycle analysis and apoptosis assays were used to determine the effect of VD3 and calcitriol-induced growth suppression in leukemic cells in vitro. Results: VD3 and calcitriol treatment strongly inhibited cancer progression in a mouse model of erythroleukemia induced by the Friend virus. In tissue culture, VD3 and calcitriol inhibited cell proliferation of leukemia cell lines. This leukemic inhibition was associated with the induction of G1 phase cell cycle arrest and apoptosis. Interestingly, RNAseq analysis supported by RT-qPCR revealed that both VD3 and calcitriol induced most known genes associated with the metabolic pathway in leukemic cells. The transcription of the VD3 receptor VDR is strongly induced by both VD3 and calcitriol treated cells. However, leukemia growth suppression by VD3/CA is shown to be independent of the activation of VDR. However, these compounds appeared to suppress the oncogene NOTCH1 by upregulating the cytosolic glutathione degradase CHAC1. Accordingly, lentivirus-mediated knockdown of CHAC1 antagonized leukemia cell suppression induced by VD3 and calcitriol, associated with higher NOTCH1 activation compared to control. Lentivirus-mediated overexpression of CHAC1 suppressed leukemia cell growth and inhibited the expression of NOTCH1. Additionally, glutathione antagonized leukemia cell suppression induced by VD3 and calcitriol, suggesting further that VD3 and calcitriol may inhibit the proliferation of leukemic cells by regulating the CHAC1 pathway. Conclusions: These results demonstrated strong anti-leukemia activity of VD3 and Calcitriol. Moreover, the above results implicated CHAC1-mediated NOTCH1 suppression as the mechanism of leukemia cell growth inhibition by VD3 and calcitriol.
2025-07-01 | GSE270534 | GEO
Project description:We used ChIP-Seq to identify the genomic locations bound by the vitamin D receptor (VDR) in two lymphoblastoid cell lines (LCLs) (CEPH individuals GM10855 and GM10861 from the International HapMap Project) before and after calcitriol treatment for 36 hours. Immunoprecipitated DNA was sequenced using the Illumina Genome Analyzer II. Sequence reads (35 bases; 10-19 million quality-filtered reads/sample) were aligned to the human genome (NCBI Build 36.3) using ELAND software. The number of unique alignments ranged from 7.73 million to 14.32 million. Peaks were called in the aligned sequence data using a model-based analysis of ChIP-Seq (MACS) and compared with sequenced sonicated and amplified input DNA. In the samples not treated with calcitriol, the number of peaks ranged from 468 to 4538 (median 975, mean 1587), while in the calcitriol-treated samples the number of peaks was between 2560 and 7244 (median 4546, mean 4560). 65-75% of peaks of untreated samples were in promoters, while only 24-50% of peaks of calcitirol-treated samples were in promoters. This study provides a comprehensive map of VDR binding in lymphoblastoid cell lines. The GM10855 and GM10861 cell lines were either stimulated for 36 hours with calcitriol or unstimulated, and crosslinked with formaldehyde to generate a snapshot of all protein-DNA interactions occurring in the nucleus at that particular point in time. Antibodies were then used to immunoprecipitate the VDR protein together with the crosslinked DNA fragments. Following reversal of crosslinks and digestion of protein, adaptors were ligated to immunoprecipitated DNA, and bridge PCR was used to generate clonally amplified amplicons before sequencing by synthesis using the Illumina Solexa Genome Analyzer.
2010-06-22 | E-GEOD-22484 | biostudies-arrayexpress
Project description:evaluate the impact of fecal sample preparation protein digestion data acquisition mode and bioinformatic workflow on metaproteomic observations
2024-07-03 | PXD049086 | Pride