Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA229371 | ENA |
REPOSITORIES: ENA
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Project description:Compared gene expression in lymphoblasoid cell lines from alcholics and controls and 24 hr treatment with ethanol. To elucidate the effects of a controlled exposure to ethanol on gene expression, we studied lymphoblastoid cell lines (LCLs) from 21 alcoholics and 21 controls. We cultured each cell line for 24 h with and without 75 mM ethanol and measured gene expression using microarrays. Differences in expression between LCL from alcoholics and controls were modest, but included 13 genes previously identified as associated with alcoholism or related traits in one or more GWAS, including KCNA3, DICER1, ZNF415, Catalase and PPARGC1B. The paired design allowed us to detect very small changes due to ethanol treatment: ethanol altered the expression of 37% of the probe sets (51% of the unique named genes) detectably expressed in these LCLs, but most by very modest amounts. 99% of the named genes expressed in the LCLs were also expressed in at least 1 of 9 brain regions tested, suggesting that LCLs are a reasonable and accessible proxy for brain tissues. Key pathways affected by ethanol include cytokine, TNF and NF-kB signaling. Among the genes affected by ethanol were ANK3, EPHB1, SLC1A1, SLC9A9, NRD1, and SH3BP5, which were reported to be associated with alcoholism or related phenotypes in 2 genome wide association studies. Genes that either differed in expression between alcoholics and controls or were affected by ethanol exposure are candidates for further study. Lymphoblastoid cells from 21 alcoholics and 21 controls were treated with 75mM ethanol for 24 hours.
2014-10-22 | E-GEOD-52553 | biostudies-arrayexpress
Project description:Breast cancer is the second leading cause of cancer-related deaths in women (*). Many genetic and behavioral risk factors can contribute to the initiation and progression of breast cancer, one being alcohol consumption. Numerous epidemiological studies have established a positive correlation between alcohol consumption and breast cancer; however, the molecular basis for this link remains ill defined. Elucidating ethanol-induced changes to global transcriptional programming in breast cells is important to ultimately understand how alcohol and breast cancer are connected mechanistically. We investigated early induced transcriptional changes in response to cellular exposure to moderate levels of alcohol. We treated the non-tumorigenic breast cell line MCF10A, and the tumorigenic breast cell lines MDA-MB-231 and MCF7, with ethanol for 6 h, then captured the changes to ongoing transcription using 4-thiouridine metabolic labeling followed by deep sequencing. Only the MCF10A cell line exhibited statistically significant changes to ongoing transcription in response to ethanol treatment. Further experiments revealed some ethanol-upregulated genes are sensitive to the dose of alcohol treatment, while others are not. Gene ontology and biochemical pathway analyses revealed that ethanol-upregulated genes in MCF10A cells are enriched in biological functions that could contribute to cancer development.
2023-08-04 | GSE221280 | GEO
Project description:The goal for this study was to determine the effects of ethanol on pancreas cells and examine how ethanol influences protein expression in non-transformed and mutant KRAS cells. We performed TMT-labeled proteomics of non-transformed (hTERT-HPNE E6/E7) and KRAS mutated (hTERT-HPNE E6/E7/K-RasG12D) human pancreas cell lines following 6 months of 100 mM ethanol treatment.
2022-05-19 | PXD030180 | Pride
Project description:Compared gene expression in lymphoblasoid cell lines from alcholics and controls and 24 hr treatment with ethanol. To elucidate the effects of a controlled exposure to ethanol on gene expression, we studied lymphoblastoid cell lines (LCLs) from 21 alcoholics and 21 controls. We cultured each cell line for 24 h with and without 75 mM ethanol and measured gene expression using microarrays. Differences in expression between LCL from alcoholics and controls were modest, but included 13 genes previously identified as associated with alcoholism or related traits in one or more GWAS, including KCNA3, DICER1, ZNF415, Catalase and PPARGC1B. The paired design allowed us to detect very small changes due to ethanol treatment: ethanol altered the expression of 37% of the probe sets (51% of the unique named genes) detectably expressed in these LCLs, but most by very modest amounts. 99% of the named genes expressed in the LCLs were also expressed in at least 1 of 9 brain regions tested, suggesting that LCLs are a reasonable and accessible proxy for brain tissues. Key pathways affected by ethanol include cytokine, TNF and NF-kB signaling. Among the genes affected by ethanol were ANK3, EPHB1, SLC1A1, SLC9A9, NRD1, and SH3BP5, which were reported to be associated with alcoholism or related phenotypes in 2 genome wide association studies. Genes that either differed in expression between alcoholics and controls or were affected by ethanol exposure are candidates for further study.
2014-10-22 | GSE52553 | GEO
Project description:Microglia, the resident immune cells of the brain, can exhibit a broad range of activation phenotypes, many of which have been implicated in several diseases and disorders of the central nervous system including alcohol use disorders and disorders. By utilizing a method optimized for sensitive and rapid quantitative proteomic analysis of microglia involving suspension trapping (S-Trap), we were able to produce efficient and reproducible protein extraction from low cell yielding primary mouse brains. Using a ~2 h gradient on a 75 cm UPLC column with a modified data dependent acquisition method on a hybrid quadrupole-Orbitrap mass spectrometer (QE Plus), 5,062 total proteins were identified where 4,928 of those proteins were quantifiable by label-free quantitation (with 5 biological replicates). This analysis resulted in the most comprehensive proteomic dataset for ethanol- and LPS-treated primary mouse microglia to date and even expanded upon the well-characterized macrophage/microglia response to LPS treatment. This study also highlights the subtle, yet significant changes ethanol exposure can induce when compared to control. Interestingly, these changes are not consistent with the robust classical activation induced by LPS treatment, but instead align with the emerging theory that ethanol-treated microglia yield an alternative activation response. The contrast to LPS-treated microglia leads us to conclude that ethanol does not elicit a strong inflammatory response but rather might have a general inhibitory effect on multiple pathways such as phagocytosis and cell migration.
2020-04-07 | PXD014466 | Pride
Project description:Gene expression studies were performed to identify pathways possibly dysregulated by mutant in the gene Gα(olf). These experiments employed RNA derived from lymphoblastoid cell lines established for 4 affected carriers and 4 non-carriers. In comparison to endogenous control and other dystonia-associated genes, GNAL was expressed at relatively low levels in lymphoblastoid cell lines.
2013-01-26 | GSE43771 | GEO
Project description:Microarray-based gene expression analysis identified genes differentially expressed in 3 MCL and 3 CLL cell lines compared to the lymphoblastoid non-tumor cell line LCL_WEI.
2010-06-03 | GSE16412 | GEO
Project description:We used bulk RNAseq to analyze gene expression changes in six lymphoblastoid cell lines before and after incubation with busulfan
2023-06-15 | GSE178497 | GEO
Project description:Phenotypic variability is a hallmark of diseases involving chromosome gains and losses, such as Down Syndrome and cancer. Allelic variances have been thought to be the sole cause of this heterogeneity. Here, we systematically examine the consequences of gaining and losing single or multiple chromosomes to show that the aneuploid state causes non-genetic phenotypic variability. Yeast cell populations harboring the same defined aneuploidy exhibit heterogeneity in cell cycle progression and response to environmental perturbations, which we show to be partly due to gene copy number imbalances. Thus, subtle changes in gene expression severely impact the robustness of biological networks and cause alternate behaviors when they occur at a large scale. Because trisomic mice also exhibit variable phenotypes, we further propose that non-genetic individuality is a universal characteristic of the aneuploid state that could contribute to variability in presentation and treatment responses of diseases caused by aneuploidy.
2017-04-10 | PXD006009 | Pride