The prandial status modifies the associations of BMI and fatty acids with DNA methylation in men
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE140692 | GEO | 2019/12/02
REPOSITORIES: GEO
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Project description:The prandial status modifies the associations of BMI and fatty acids with DNA methylation in men
| PRJNA590522 | ENA
Project description:We have previously shown that blood global DNA methylation (DNAm) differs between postprandial state (PS) and fasting state (FS) and is associated with BMI and polyunsaturated fatty acid (PUFA) (negatively and positively, respectively) in 12 metabolically healthy adult Mexican men (AMM cohort) equally distributed among conventional BMI classes. Here, we detailed those associations at CpG dinucleotide level by exploiting the Infinium methylation EPIC array (Illumina). We sought differentially methylated CpG (dmCpG) that were (1) associated with BMI (BMI-dmCpG) and/or fatty acids (FA) (FA-dmCpG) in FS or PS and (2) different across FS and PS within a BMI class. BMI-dmCpG and FA-dmCpG were more numerous in FS compared to PS and largely prandial state-specific. For saturated and monounsaturated FA, dmCpG overlap was higher across than within the respective saturation group. Several BMI- and FA-dmCpG mapped to genes involved in metabolic disease and in some cases matched published experimental data sets. Notably, SETDB1 and MTHFS promoter dmCpG could explain the previously observed associations between global DNAm, PUFA content, and BMI in FS. Surprisingly, overlap between BMI-dmCpG and FA-dmCpG was limited and the respective dmCpG were differentially distributed across functional genomic elements. BMI-dmCpG showed the highest overlap with dmCpG of the saturated FA palmitate, monounsaturated C20:1 and PUFA C20:2. Of these, selected promoter BMI-dmCpG showed opposite associations with palmitate compared to C20:1 and C20:2. As for the comparison between FS and PS within BMI classes, dmCpG were strikingly more abundant and variably methylated in overweight relative to normoweight or obese subjects (∼70-139-fold, respectively). Overweight-associated dmCpG-hosting genes were significantly enriched in targets for E47, SREBP1, and RREB1 transcription factors, which are known players in obesity and lipid homeostasis, but none overlapped with BMI-dmCpG. We show for the first time that the association of BMI and FA with methylation of disease-related genes is distinct in FS and PS and that limited overlap exists between BMI- and FA-dmCpG within and across prandial states. Our study also identifies a transcriptional regulation circuitry in overweight that might contribute to adaptation to that condition or to transition to obesity. Further work is necessary to define the pathophysiological implications of these findings.
| S-EPMC8138173 | biostudies-literature
Project description:Over-expression of the polycomb group gene BMI-1 is implicated in the pathogenesis of many human cancers. In this study, we investigate the role of BMI-1 as a functional oncogene in the Ewing’s Sarcoma Family of Tumors (ESFT), a highly aggressive group of bone and soft tissue tumors. Our data show that BMI-1 is highly expressed by the majority of primary ESFT and ESFT cell lines. However, in contrast to previous reports in other human cancer cell types, knockdown of BMI-1 in ESFT cell lines has no effect on cell survival. Instead, gain and loss of function studies in vitro and in vivo demonstrate that BMI-1 promotes the anchorage independent growth and tumorigenicity of ESFT. Importantly, we also find that modulation of BMI-1 alters the tumorigenicity of both p16-wild type and p16-null cell lines and that BMI-1-mediated effects on growth promotion are independent of CDKN2a repression. Gene expression profiling of ESFT cells following BMI-1 modulation reveals novel downstream effectors of BMI-1 function including key developmental, cell:cell and cell:matrix adhesion pathways. These data support a central role for BMI-1 in the pathogenesis of ESFT and reveal that p16-independent functions of BMI-1 are largely responsible for its oncogenic function in this tumor family. Keywords: Modification of BMI-1 expression in ESFT cell lines
2008-07-18 | GSE12064 | GEO
Project description:We measured genes expression differences in antibody secreting cells from LynKO mice in following treatment with a BMI-1 inhibitor (PTC-028) or a vehicle control. BMI-1 inhibition lead to a reduction in antibody secreting cells in LynKO mice and in humans donors. We performed RNA sequencing to understand the impact of BMI-1 inhibition on antibody secreting cells in LynKO mice.
2023-10-05 | GSE239515 | GEO
Project description:Our studies demonstrate that BMI-1 plays a crucial role in the EMT process and drug resistance in melanoma. Silencing Bmi-1 significantly inhibites the aggressive behavior and improves the chemosensitivity to all-trans retinoic acid on melanoma cells. We compared the different genes expression of A375-vector and A375-BMI-1 cells for exploring the underlying mechanisms of BMI-1 regulation on melanoma.
2021-06-01 | GSE115644 | GEO
Project description:One current focus of nutrition research is the identification of biomarkers that reflect the impact of food on metabolic processes. As this approach mostly targets the prevention rather than the curing of diseases, novel biomarkers need to be identified. Those should be influenced by the diet already in healthy individuals and be nonetheless indicative, or even predictive, of the potential impact of specific food on the development of metabolic diseases such as obesity. The blood cell transcriptome of two different population groups after the ingestion of different caloric doses of a high-fat meal was measured by microarray technology.
2017-03-14 | GSE56960 | GEO
Project description:Brucella microti HUN-Bmi-01 genome sequencing
| PRJNA272528 | ENA
Project description:The goal of this study is to identify genes that are differentially expressed by E6 in oral epithelial cells that are stably expressing Bmi-1. Keywords: oncogenesis.
2006-10-20 | GSE6075 | GEO
Project description:The critical role of Bmi1 in promoting stem cell properties has been shown in different type of human cancers. Here, we established four stable clones to study Bmi-regulated miRNA expression patterns in head and neck caners. Bmi1-overexpressing cell lines (FaDu- Bmi1vs. FaDu-pcDNA3 cell line), and knock-down of Bmi1 cell lines (OECM1-sh-Bmi vs. OECM1-sh-Bmi1 cell lines) were established and used for analyzing miRNA expression patterms in Bmi-regulatory mechanism.
2013-02-11 | E-GEOD-31910 | biostudies-arrayexpress
Project description:Bmi-1 and Mel-18 are close structural homologues that belong to the polycomb group (PcG) of transcriptional regulators of homeotic gene expression in development. They are believed to stably maintain repression of gene expression by altering the state of chromatin at specific promoters. A number of clinical and experimental observations have also implicated Bmi-1 in tumorigenesis and stem cell maintenance. Bmi-1 overexpression or amplification has been observed in a number of human malignancies, particularly in B-cell lymphomas, medulloblastomas and breast cancer. We report here that shRNA-mediated knock-down of either Bmi-1 or Mel-18 in human medulloblastoma DAOY cells results in the inhibition of proliferation, loss of clonogenic survival and anchorage-independent growth, and suppression of xenograft tumor formation in nude mice. Furthermore, overexpression of both Bmi-1 and Mel-18 significantly increased clonogenic survival of Rat1 fibroblasts. In contrast, stable downregulation of Bmi-1 or Mel-18 alone did not affect the growth of SK-OV-3 or U2OS cancer cell lines or normal human WI38 fibroblasts. Gene expression analysis of shRNA-expressing DAOY cells has demonstrated a significant overlap in the Bmi-1- and Mel-18-regulated genes and revealed novel gene targets under their control. Taken together, these results suggest that Bmi-1 and Mel-18 might have overlapping functions in human tumorigenesis. Keywords: shRNA knock-down
2007-05-01 | GSE7578 | GEO