Gene alteration in A549 cells by disinfectant PHMG
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Kim Yong-Sik
PROVIDER: S-ECPF-GEOD-41156 | biostudies-other |
REPOSITORIES: biostudies-other
Similar Datasets
Project description:Polyhexamethyl guanidine is widely used as a disinfectant in various places such as hospitals and restaurants. In order to examine of PHMG cytotoxicity in lung adenocarcinoma A549 cells we treated 5 ug/ml PHMG for 24 h. To investigate cytotoxicity of commonly used bactericidal reagent PHMG, A549 cells were treated 5 ug/ml PHMG for 24 h. After then purified the total RNA from treated and untreated cells using the Rneasy mini kit (Qiagen). The concentration and purity of the total RNA was measured and performed gene array.
2012-09-27 | E-GEOD-41156 | biostudies-arrayexpress
Project description:Polyhexamethyl guanidine is widely used as a disinfectant in various places such as hospitals and restaurants. In order to examine of PHMG cytotoxicity in lung adenocarcinoma A549 cells we treated 5 ug/ml PHMG for 24 h.
2012-09-27 | GSE41156 | GEO
Project description:This study aimed to determine whether the radiation-induced bystander effect (RIBE) is affected by radiation quality. To mimic the different radiation qualities of the direct action (D)/indirect action (ID) ratio, A549 cells were exposed to X-rays, with either 100 mM of the radical scavenger, thio-urea (TU+), or null (TU-). Biological responses in irradiated and bystander cells were compared at equal lethal effects of a 6% survival dose, which was estimated from the survival curves to be 8 Gy and 5 Gy for TU+ and TU-, respectively. Cyclooxygenase-2 (COX-2) expression in TU- irradiated cells increased up to 8 h post-irradiation, before decreasing towards 24 h. The concentration of prostaglandin E2 (PGE2), a primary product of COX-2 and known as a secreted inducible factor in RIBE, increased over 3-fold compared with that in the control at 8 h post-irradiation. Conversely, COX-2 expression and PGE2 production of TU+ irradiated cells were drastically suppressed. These results show that the larger D/ID suppressed COX-2 expression and PGE2 production in irradiated cells. However, in contrast to the case in the irradiated cells, COX-2 expression was equally observed in the TU- and TU+ co-cultured bystander cells, which showed the highest expression levels at 24 h post-irradiation. Taken together, these findings demonstrate that radiation quality, such as the D/ID ratio, may be an important factor in the alteration of signalling pathways involved in RIBE.
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Project description:Expansion of nanotechnology will bring many potential benefits as adversely effects on human health. Protection of the human respiratory system from exposure of volatile nanoparticles has become an emerging health concern. The understanding of the biological processes involved in the development and maintenance of a variety of pathologies is improved by genome-wide approaches. Technical feasibility of this type of experiment has perfected in recent years, but data analysis remains challenging. In this context, gene set analysis has emerged as a fundamental tool for the interpretation of the results. We demonstrate how the use of a combination of gene-by-gene and gene set analyses can enhance the interpretation of results. Gene set analyses are able to distinguish responses due to nanoparticle size also discriminating between long and short time recovery after exposure. Transcription regulation and cell proliferation modulation appear to be an early response while oxidative stress and mitochondrial perturbation are late response. Moreover, smaller the particle higher the effect on inflammatory response and DNA damage activation. By integrating the two approaches, we evidenced the importance of MMP1, MMP9, MMP7 and MMP14 genes in response to Ludox® silica nanoparticles and the involvement apoptosis process in cell viability. This study is based on the treatment of A549 cells with two different silica nanoparticles (SM30, 9 nm of diameter, and AS30, 18 nm of diameter). Treatment with nanoparticles were performed independently. We performed three biological replicates for each condition.
| S-ECPF-GEOD-53700 | biostudies-other
Project description:The aim of the present study was to investigate the effects of transketolase (TKT) on cell proliferation, cell migration and interaction with other metabolism-associated genes in A549 lung cancer cells. A549 cells were transfected with three TKT-specific small interfering (si)RNAs, screened for the optimal transfection concentration, and sequenced with flow cytometry and reverse transcription-quantitative polymerase chain reaction (RT-qPCR). Cell viability was evaluated using Cell Counting Kit-8 (CCK-8), cell cycle was assessed by flow cytometric analysis. Cell migration was determined by scratch-wound and Transwell chamber assays. The changes in mRNA expression levels of glucose-6-phosphate dehydrogenase (G6PDH), transaldolase (TAL), sorbitol dehydrogenase (SORD), phosphoribosyl pyrophosphate synthetase 1 (PRPS1) and hexokinase 1 (HK1) were detected by RT-qPCR. siRNA-C at 50 nmol/l was selected for the subsequent experiments. Compared with the negative control, cell proliferation of the TKT-siRNA-C group was inhibited dramatically (CCK-8 24 h, 0.2984±0.0371 vs. 0.0952±0.0063; P<0.0001), the cell cycle was arrested at the G1/G0 cell cycle phase (58±2.0% vs. 70±2.5%; P=0.002), and cell migration ability was decreased [wound size, 254.71±34.96 vs. 349.12±37.43 µm (P=0.0001); Transwell migration, 250±47.8/field vs. 150±49.0/field (P<0.0001)]. The mRNA expression levels of G6PDH, TAL, SORD, PRPS1 and HK1 were downregulated in the TKT-siRNA-C group compared with the negative control. The present study revealed that synthetic TKT-siRNA can inhibit A549 cell viability and migration, which may be due to arrest of the cell cycle and downregulation of relevant metabolic enzymes.
| S-EPMC5661397 | biostudies-literature
Project description:BackgroundThe studies on cancer-stem-cells (CSCs) have attracted so much attention in recent years as possible therapeutic implications. This study was carried out to investigate the gene expression profile of CSCs in human lung adenocarcinoma A549 cells.ResultsWe isolated CSCs from A549 cell line of which side population (SP) phenotype revealed several stem cell properties. After staining the cell line with Hoechst 33342 dye, the SP and non-side population (non-SP) cells were sorted using flow cytometric analysis. The mRNA expression profiles were measured using an Affymetrix GeneChip(R) oligonucleotide array. Among the sixty one differentially expressed genes, the twelve genes inclusive three poor prognostic genes; Aldo-keto reductase family 1, member C1/C2 (AKR1C1/C2), Transmembrane 4 L six family member 1 nuclear receptor (TM4SF1), and Nuclear receptor subfamily 0, group B, member 1 (NR0B1) were significantly up-regulated in SP compared to non-SP cells.ConclusionThis is the first report indicating the differences of gene expression pattern between SP and non-SP cells in A549 cells. We suggest that the up-regulations of the genes AKR1C1/C2, TM4SF1 and NR0B1 in SP of human adenocarcinoma A549 cells could be a target of poor prognosis in anti-cancer therapy.
| S-EPMC2234429 | biostudies-literature
Project description:Gene expression profiling was analyzed using A549 cells that were treated with glucose deprivation (GD) or GD + phorbol-12-myristate-13-acetate (PMA). Gene expression levels were determined by comparing the gene expression of the experimental samples (GD or GD+PMA) with that of the control sample.
| S-ECPF-GEOD-24271 | biostudies-other
Project description:Embelin (15 uM) induced alterations in the gene expression profile was studied in A549 lung cancer cells during the initial stages of apoptosis (4h following treatment) As embelin (15 uM) induces apoptosis as early as 4h time period, we performed microarray analysis to study embelin-induced differential gene expression as early as 4h to identify the responsible pathways.
| S-ECPF-GEOD-50545 | biostudies-other
Project description:Propofol (2,6-diisopropylphenol) is one of the most commonly used intravenous anesthetics and possesses a number of non-anesthetic effects, including antitumor function. The aim of the present study was to elucidate the antitumor molecular mechanism of propofol on A549 and H1299 cells. A549 and H1299 cells were treated in the presence or absence of different concentrations (0, 60 or 120 µmol) of propofol for different durations (0, 24, 48 or 72 h), and proliferation was detected by MTT and colony formation assays; the protein levels of optineurin (OPTN) ubiquitination, HECT domain and ankyrin repeat containing E3 ubiquitin protein ligase 1 (HACE1), methyl-CpG binding domain protein 3 (MBD3) and Microtubule-associated protein 1A/1B-light chain 3 were detected by immunoblotting or quantitative (q)PCR; the methylation state of the HACE1 gene promoter was detected by bisulfite DNA sequencing; and binding of MBD3 on HACE1 gene promoter was detected by chromatin immunoprecipitation-qPCR. Propofol inhibited proliferation of A549 and H1299 cells and promoted HACE1-OPTN axis-mediated selective autophagy activity by increasing the protein expression levels of HACE1 via demethylating its promoter region. Furthermore, propofol promoted expression levels of MBD3 and binding to the -1,000 to -1 bp (transcription start site) region of HACE1 gene promoter. MBD3-knockdown experiments indicated that propofol inhibited proliferation of A549 cells in a MBD3-dependent manner. Thus, the findings of the present study provided a potential antitumor molecular mechanism mediated by propofol.
| S-EPMC7520799 | biostudies-literature
Project description:To evaluate gene expression alteration following miR-139-5p transfection in glioma cells. We find a significant downregulation of two transcriptional factors, E2F3 and HoxA9. Total RNA were extracted from U87, LN229 and U251 glioma cells transfected with miR-139-5p or miRNA negative control.
| S-ECPF-GEOD-44728 | biostudies-other