Homo sapiens
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ABSTRACT:
PROVIDER: PRJNA101743 | ENA |
REPOSITORIES: ENA
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Project description:Affymetrix high-density oligonucleotide microarray analysis was performed to analyse hydroxylated polybrominated diphenyl ethers (OH-PBDE)-induced gene expression changes in H295R adrenocortical carcinoma cells. Cells were treated with growth medium in the presence or absence of 10 µM 2-OH-BDE47 or 2-OH-BDE85 for 24 hours before the gene expression changes were investigated. Experiment Overall Design: Gene expression changes in response to hydroxylated polybrominated diphenyl ethers (OH-PBDEs) were analysed by Microarray technology in H295R adrenocortical carcinoma cells. Cells were treated with 10 µM of 2-OH-BDE47 or 2-OH-BDE85 (or growth medium alone) for 24 hours before the OH-PBDE-induced gene expression changes were investigated. Control, 2-OH-BDE47- and 2-OH-BDE85-treated samples were collected from three independent experiments each.
2009-01-02 | E-GEOD-8588 | biostudies-arrayexpress
Project description:Polybrominated diphenyl ethers (PBDEs) are commonly used as flame retardants in a variety of commercial and household products. They have been detected in the environment and accumulate in mammalian tissues and fluids. PBDE toxicity is thought to be associated with endocrine disruption, developmental neurotoxicity and changes in fetal development. Although humans are exposed to PBDEs, our knowledge of the effects of PBDE metabolites on human cells with respect to health risk is insufficient. Two hydroxylated PBDEs (OH-PBDEs), 2-OH-BDE47 and 2-OH-BDE85, were investigated for their effects on cell viability/proliferation, DNA damage, cell cycle distribution and gene expression profiling in H295R adrenocortical carcinoma cells. We show that the two agents are cytotoxic in a dose-dependent manner only at micromolar concentrations, with 2-OH-BDE85 being more toxic than 2-OH-BDE47. However, no DNA damage was observed for either chemical, suggesting that the biological effects of OH-PBDEs occur primarily via non-genotoxic routes. Furthermore, no evidence of aryl hydrocarbon receptor (AHR)-mediated, dioxin-like toxicity was observed. Instead, we report that a micromolar concentration of OH-PBDEs induces transcriptional changes associated with endoplasmic reticulum stress and the unfolded protein response. We discuss whether OH-PBDE bioaccumulation could result in impairment of the adrenocortical secretory function.
2008-12-25 | GSE8588 | GEO
Project description:Adrenocortical carcinoma is a rare tumour with a poor prognosis. The currently available medical treatment options of adrenocortical cancer are limited. In the present study we examine the potential antitumoral effects of 9-cis-retinoic acid (9-cisRA) on the adrenocortical cancer cell line NCI-H295R. For the gene expression profiling, H295R cells were treated for 24h with 9cisRA at a final concentration of 2.5*10-5, 5*10-5 and 7.5*10-5 M and for the contol with the same amount of ethanol.
2013-02-10 | E-GEOD-43090 | biostudies-arrayexpress
Project description:The actin-bundling protein fascin (FSCN1) is overexpressed in aggressive adrenocortical carcinoma (ACC) and represents a reliable prognostic indicator. We investigated the effects of FSCN1 inactivation by CRISPR/Cas9 in ACC H295R cells on global gene expression profiles in those cells. We performed gene expression profiling analysis using data obtained from RNA-seq of 2 different H295R control clones and 2 different FSCN1 KO clones (2 biological replicates for each clone).
2022-10-25 | GSE216008 | GEO
Project description:Transcription factor 21 (TCF21) directly binds and regulates SF1 in tumor and normal adrenocortical cells, and both are involved in the development and steroidogenesis of the adrenal cortex. TCF21 is a tumor suppressor gene and its expression is reduced in malignant tumors. In adrenocortical tumors, it is less expressed in adrenocortical carcinomas (ACC) than in adrenocortical adenomas (ACA) and normal tissue. However, a comprehensive analysis to identify TCF21 targets have not yet been conducted in any type of cancer. In this study, we performed Chromatin Immunoprecipitation and Sequencing (ChIP-Seq) in adrenocortical carcinoma cell line (NCI-H295R) overexpressing TCF21, with the aim of identifying TCF21 new targets. The five most frequently identified sequences corresponded to the PRDM7, CNTNAP2, CACNA1B, PTPRN2 and KCNE1B genes. Validation experiments showed that, in NCI-H295R cells, TCF21 regulates gene expression positively in PRDM7 and negatively in CACNA1B. Recently, it was observed that the N-type calcium channel v2.2 (Cav2.2) encoded by CACNA1B gene is important in Angiotensin II signal transduction for corticosteroid biosynthesis in NCI-H295R adrenocortical carcinoma cells. Indeed, TCF21 inhibits CACNA1B and Cav2.2 expression in NCI-H295R. In addition, in a cohort of 55 adult patients with adrenocortical tumor, CACNA1B expression was higher in ACC than ACA, and was related to poor disease-free survival in ACC patients. These results suggest a mechanism of steroidogenesis control by TCF21 in adrenocortical tumor cells, in addition to the control observed through SF1 inhibition. Importantly, steroid production could impair tumor immunogenicity, contributing to the immune resistance described in adrenal cancer.
2022-06-30 | GSE179308 | GEO
Project description:Adrenocortical carcinoma is a rare tumour with a poor prognosis. The currently available medical treatment options of adrenocortical cancer are limited. In the present study we examine the potential antitumoral effects of 9-cis-retinoic acid (9-cisRA) on the adrenocortical cancer cell line NCI-H295R.
2013-02-10 | GSE43090 | GEO
Project description:Despite the intensive search for an effective drug to ameliorate excess steroid production, there are few pharmacological options, especially for diseases as steroid-producing adrenocortical cancers. While splice-modifying-compounds have pleiotropic effects including anticancer properties, none have been tested on abnormal steroidogenesis. Using H295R adrenocortical carcinoma cells, CX-4945 induced multiple exon skipping of the NR5A1 gene, the master regulator of steroidogenesis. The resulting exon-skipped NR5A1 proteins were non-functional when added-back to NR5A1 knocked down H295R cells. This eventually suppressed steroidogenesis and induced dysfunctional autophagy with progression to ER-stress-related apoptosis. Intriguingly, a circular RNA of NR5A1 exons (circNR5A1 ex2-4 RNA) not originating from the skipped exons, was induced. Transient expression of this circNR5A1 ex2-4 RNA induced the same multiple exon-skipped isoforms of the NR5A1 gene. This potential pharmacological control of NR5A1 aberrant multiple exon-skipping and interplay with its circNR5A1 RNA gives us a novel target for treating abnormal steroidogenesis in adrenocortical carcinomas.
2022-06-24 | GSE133197 | GEO
Project description:Angiotensin II early regulated genes in H295R human adrenocortical cells
| PRJNA87099 | ENA
Project description:H295R human adrenocortical cells treated with Angiotensin II, Potassium or Forskolin
| PRJNA96051 | ENA
Project description:The human adrenocortical carcinoma cell line NCI-H295R treated with siRNA targeting SF-1 or RNF31 with luciferase-targeting siRNA as control. Combined with forskolin treatment.
2012-02-01 | E-MEXP-3259 | biostudies-arrayexpress