Ontology highlight
ABSTRACT:
PROVIDER: PRJNA791172 | ENA |
REPOSITORIES: ENA
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Project description:5α-androstane-3α,17β-diol (3α-diol) is reduced from the potent androgen, 5α-dihydrotestosterone (5α-DHT), by reductive 3α-hydroxysteroid dehydrogenases (3α-HSDs). 3α-diol is believed to be a weak androgen, and has to be oxidized to 5α-DHT before it can exert its androgenic activity on androgen target tissues including the prostate. However, we repeatedly demonstrated that 3α-diol can be a potent androgen, activates cytoplasmic signaling pathway, and may be responsible for androgen-independent prostate cancer growth. A cancer-specific, cDNA-based membrane array was used to determine 3α-diol-mediated gene expressions in prostate cancer progression. Several canonical pathways appeared to be affected by 3α-diol-regulated signaling in LNCaP cells; among them are apoptosis signaling, PI3K/Akt signaling, and death receptor signaling pathways. Biological analysis of 3α-diol-activated signaling confirmed that 3α-diol augmented PI3K/Akt activation can be independent from the classical androgen receptor (AR) signaling. These observations sustained our previous report that 3α-diol continues to supported prostate cell survival and proliferation regardless the status of the AR. We provided the first global analysis of 3α-diol-activated gene expressions and identified cytoplasmic signaling pathways as important components of this response in human prostate cells. 3α-diol may play, therefore, a significant role for transition from androgen-dependent to androgen-independent prostate cancer progression in the presence of androgen blockade. Keywords: array, time course, androgen, prostate, cancer
2008-08-01 | GSE8860 | GEO
Project description:Estrogen Receptor-alpha (ER) is the key driver of 75% of all breast cancers. Upon stimulation by its ligand estra-2-diol, ER forms a transcriptionally active complex binding chromatin. Previous studies have reported that ER binding follows a cyclical binding pattern with a periodicity of 90 minutes. However, these studies have been limited to individual ER target genes and most were done without replicates. Thus, the robustness and generality of ER cycling are not well understood. Here we present a comprehensive genome-wide analysis of the time dependence of ER binding affinity up to 90 minutes after activation, based on 6 replicates at 10 time points using our previously reported method for precise quantification of binding, Parallel-Factor ChIP-seq (pfChIP-seq). In contrast to previously described cyclical binding, our approach identifies a unidirectional sustained increase in ER binding affinity, as well as a class of estra-2-diol independent binding sites. Our results are corroborated by a quantitative re-analysis of data from multiple independent studies. Our new model reconciles the results of multiple conflicting studies into the activation of ER at the TFF1 promoter. We provide a detailed understanding of ER's response to estra-2-diol in the context of the receptor's fundamental role as both the main driver and therapeutic target of breast cancer
2018-08-28 | GSE119057 | GEO
Project description:Herein, we evaluated the regulation of plantaricin NC8 on gut microbiota by in vitro simulation system, and assessed their modulation on different intestinal types, namely enterotype 1 (ET B) and enterotype 2 (ET P), for the first time. Plantaricin NC8 could not significantly promote or inhibit the production short chain fatty acids (SCFAs) by the gut flora in the fecal samples from eight subjects to produce through Gas chromatography (GC) determining, neither ET B nor ET P. 16S rDNA sequencing showed that plantaricin NC8 shortened the Shannon index of ET B and the Simpson index of ET P, but their β diversity change was not statistically significant. In addition, plantaricin NC8 could promote the growth of beneficial bacteria. Results showed that plantaricin NC8 mainly increased the abundance of Actinobacterias, Bacteroides, Bifidobacterium, Megamonas, Escherichia-Shigella, and decreased the abundance of Streptococcus in ET B. And it also increased the abundance of Prevotella_9, Bifidobacterium, Escherichia-Shigella, Mitsuokella and others in ET P. Plantaricin NC8 can influence intestinal microorganisms, but the influence were different for different enterotypes.
2022-03-30 | GSE199735 | GEO
Project description:PURPOSE: To develop an index capable of detecting and quantifying the extent of liver RNA contamination in liver biopsies of metastatic breast cancer METHODS: We developed a microarray-based gene expression liver index by comparing the expression levels of genes in liver tissue biopsies and in primary breast cancer biopsies. The predictive performance of the index was then evaluated in defined mixtures of liver and breast cancer RNA. A calibration curve was established to allow estimation of the liver RNA content in unknown metastatic breast cancer samples.
2013-01-05 | GSE33116 | GEO
Project description:Global gene expression analysis of HCC1428-LTED (long term estrogen deprived) breast cancer cell lines was evaluated after overnight treatment with 6 selective estrogen receptor degarders (SERDs). Two gene expression signatures were identified. GDC-0810 and AZD9496 have a similar gene expression profile which is distinct from fulvestrant. SAR439859 gene expression signature clusters closely with fulvestrant. Replacing the carboxylic side chain of GDC-0810 and AZD9496 with a basic side chain of SAR439859 to make novel SERDs, GDC-SAR and AZD-SAR, respectively, shifts the gene expression signature to more closely align to that of fulvestrant. The effect of SERDs on gene expression can be used to further differentiate classes of SERDs.
2020-07-10 | GSE154058 | GEO
Project description:Dietary N-3 Long Chain Polyunsaturated Fatty Acids
| PRJDB8506 | ENA
Project description:The present study aims to explore the expression profiles and biological functions of long-chain noncoding RNA (lncRNA) in coronary heart disease (CHD)
2021-03-21 | GSE169256 | GEO
Project description:Cellular responses to carcinogens are typically studied in transformed cell lines, which do not reflect the physiological status of normal tissues. To address this question, we have characterized the transcriptional program and cellular responses of normal human lung WI-38 fibroblasts upon exposure to the ultimate carcinogen benzo[a]pyrene diol epoxide (BPDE). Exposure to BPDE induces a strong inflammatory response in WI-38 primary fibroblasts. Whole-genome microarray analysis shows induction of several genes related to the production of inflammatory factors, including those that encode interleukins (ILs), growth factors, and enzymes related to prostaglandin synthesis and signaling. This is the first demonstration that a strong inflammatory response is triggered in primary fibroblasts in response to a reactive diol epoxide derived from a polycyclic aromatic hydrocarbon.
2010-01-01 | GSE19510 | GEO