Effect of SRSF2 over-expression in a human lung carcinoma cell line
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Corcos Laurent
PROVIDER: S-ECPF-GEOD-50467 | biostudies-other |
REPOSITORIES: biostudies-other
Similar Datasets
Project description:We showed that the over-expression of the SR protein SRSF2 led to the regulation of transcript abundance of many genes.
2013-08-30 | GSE50467 | GEO
Project description:We showed that the over-expression of the SR protein SRSF2 led to the regulation of transcript abundance of many genes. H358 cell line with 6 samples with SRSF2 over-expression and 6 samples as control.
2013-08-30 | E-GEOD-50467 | biostudies-arrayexpress
Project description:Lung squamous cell carcinoma gene expression (LSCC) is highly variable. This study discovered and validated LSCC gene expression subtypes. RNA from tumors and a common reference were hybridized to Agilent two color microarrays
| S-ECPF-GEOD-17710 | biostudies-other
Project description:Esophageal squamous cell carcinoma (ESCC) is one of the most common and deadly causes of cancer worldwide. However, to date, the mechanisms underlying its pathogenesis remain unclear. The present study investigated the gene expression profile of human esophageal cancer cell line TE-1, a cell model for ESCC, to gain insight to the genetic regulation of this disease. Human esophageal cancer TE-1 cells and normal esophageal HET-1A cells were cultured for isolation of total RNA. Differential expression of RNA transcripts was assessed using the Agilent 4×44 K microarray, combined with real-time PCR (qRT-PCR) for validation. Classification and function of the differential genes were illustrated by bioinformatics processing including hierarchical clustering and gene ontology (GO) analysis. We identified 4,986 transcripts with differential expression (fold-change ≥1.5, P<0.05), including 2,368 up-regulated and 2,618 down-regulated transcripts. GO analysis showed that the dysregulated transcripts were associated with biological process, cellular component, and molecular function. After bioinformatic analysis of significantly regulated signaling pathways, we found these transcripts may target 35 gene pathways, including p53 signaling, glioma, ubiquitin-mediated proteolysis, insulin signaling, cell cycle, inositol phosphate metabolism, mTOR signaling, and MAPK signaling. The differentially expressed transcripts were screened between the esophageal cancer cell line TE-1 and normal esophageal cell line HET-1A, as well as their target gene pathways. Further data mining is related to prevention and treatment of esophageal cancer.
| S-EPMC4613095 | biostudies-literature
Project description:Paraquat (1,1'-dimethyl-4,4'-bipyridinium dichloride; PQ), an effective and widely used herbicide, was commercially introduced in 1962. It is reduced by the electron donor NADPH, and then reduced PQ transfers the electrons to molecular oxygen, resulting in the production of reactive oxygen species (ROS), which are related to cellular toxicity. However, the influence of continuous hypoxia on PQ-induced ROS production has not fully been investigated. We evaluated in vitro the protective effect of continuous hypoxia on PQ-induced cytotoxicity in the human carcinogenic alveolar basal epithelial cell line (A549 cells) by using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazolium bromide (MTT) assay and live and dead assay, and by measuring lactate dehydrogenase (LDH) release. To elucidate the mechanism underlying this effect, we monitored the immunofluorescence of intracellular ROS and measured malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione peroxidase (GPx) activities. Continuous hypoxia protected the A549 cells from PQ-induced cytotoxicity. Continuous hypoxia for a period of 24 h significantly reduced intracellular ROS, decreased MDA concentration in the supernatant, and normalized SOD and GPx activities. Continuous hypoxia attenuated PQ-induced cell toxicity in A549 cells. This protective effect might be attributable to the suppression of PQ-induced ROS generation.
| S-EPMC3203239 | biostudies-literature
Project description:BackgroundSilver nanoparticles (AgNP), the most popular nano-compounds, possess unique properties. Albizia adianthifolia (AA) is a plant of the Fabaceae family that is rich in saponins. The biological properties of a novel AgNP, synthesized from an aqueous leaf extract of AA (AA(AgNP)), were investigated on A549 lung cells. Cell viability was determined by the MTT assay. Cellular oxidative status (lipid peroxidation and glutathione (GSH) levels), ATP concentration, caspase-3/-7, -8 and -9 activities were determined. Apoptosis, mitochondrial (mt) membrane depolarization (flow cytometry) and DNA fragmentation (comet assay) were assessed. The expression of CD95 receptors, p53, bax, PARP-1 and smac/DIABLO was evaluated by flow cytometry and/or western blotting.ResultsSilver nanoparticles of AA caused a dose-dependent decrease in cell viability with a significant increase in lipid peroxidation (5-fold vs. control; p?=?0.0098) and decreased intracellular GSH (p?=?0.1184). A significant 2.5-fold decrease in cellular ATP was observed upon AA(AgNP) exposure (p?=?0.0040) with a highly significant elevation in mt depolarization (3.3-fold vs. control; p?<?0.0001). Apoptosis was also significantly higher (1.5-fold) in AA(AgNP) treated cells (p?<?0.0001) with a significant decline in expression of CD95 receptors (p?=?0.0416). Silver nanoparticles of AA caused a significant 2.5-fold reduction in caspase-8 activity (p?=?0.0024) with contrasting increases in caspase-3/-7 (1.7-fold vs. control; p?=?0.0180) and -9 activity (1.4-fold vs. control; p?=?0.0117). Western blots showed increased expression of smac/DIABLO (4.1-fold) in treated cells (p?=?0.0033). Furthermore, AA(AgNP) significantly increased the expression of p53, bax and PARP-1 (1.2-fold; p?=?0.0498, 1.6-fold; p?=?0.0083 and 1.1-fold; p?=?0.0359 respectively).ConclusionData suggests that AA(AgNP) induces cell death in the A549 lung cells via the mt mediated intrinsic apoptotic program. Further investigation is required to potentiate the use of this novel compound in cancer therapy trials.
| S-EPMC3606379 | biostudies-literature
Project description:BackgroundTo explore the molecular mechanisms of the anti-cancer effect of curcumin in human lung squamous cell carcinoma (LSQCC) SK-MES-1 cells.MethodsCell viability was determined using MTT assay. Ribonucleic acid sequencing was performed to measure expression levels of transcripts in LSQCC cells treated with 15 μmol/L curcumin (treatment groups) or an equal amount of dimethylsulfoxide (control). Cuffdiff software was used to identify differentially expressed genes (DEGs) in treatment groups, followed by enrichment analysis of DEGs using the Database for Annotation, Visualization and Integration Discovery. The protein-protein interaction (PPI) networks for up and downregulated DEGs were constructed by Cytoscape software using Search Tool for the Retrieval of Interacting Genes data to identify hub nodes.ResultsCurcumin significantly reduced cell viability in LSQCC cells. In total, 380 DEGs including 154 upregulated and 126 downregulated genes were found in the treatment groups. The upregulated genes were enriched in base excision repair (BER, such as PCNA, POLL, and MUTYH) and Janus kinase-signal transducer and activator of transcription (JAT-STAT) signaling pathways (such as AKT1 and STAT5A), while the downregulated genes were enriched in nine pathways, including the vascular endothelial growth factor (VEGF) signaling pathway (such as PTK2, VEGFA, MAPK1, and MAPK14) and mitogen-activated protein kinase (MAPK) signaling pathway (ARRB2, MAPK1, MAPK14, and NFKB1). PCNA and AKT1 were the hub nodes in the PPI network of upregulated genes while MAPK1, MAPK14, VEGFA, and NFKB1 were the hub nodes in the PPI network of downregulated genes.ConclusionsCurcumin might exert anti-cancer effects on LSQCC via regulating BER, JAT-STAT, VEGF, and MAPK signaling pathways.
| S-EPMC4511331 | biostudies-literature
Project description:The eukaryotic transcriptional Mediator comprises a large Core (cMED) and a dissociable CDK8 kinase module (CKM). cMED recruits RNA polymerase II (Pol II) and promotes pre-initiation complex formation in a manner repressed by the CKM through mechanisms presently unknown. Herein we report cryo-electron microscopy structures of the complete human Mediator and its CKM. Combined with biochemical and functional analyses, these structures provide a mechanistic framework to explain the basis for CKM-mediated repression of cMED function. The CKM binds to cMED at multiple sites through both MED12 and a large intrinsically disordered region (IDR) in MED13. The MED13 IDR blocks Pol II/MED26 recruitment onto cMED by direct occlusion of their corresponding binding sites, leading to functional repression of cMED-dependent transcription. Notably, the CKM is anchored to the cMED Hook, positioning CDK8 downstream and proximal to the transcription start site, which sheds new light on its stimulatory function in post-initiation events.
2024-12-01 | GSE250492 | GEO
Project description:M059J and M059K cells were isolated from different portions of the same human malignant glioma. M059J cells are more radiosensitive than M059K cells due to the absence of DNA-PKcs and low-expression of ATM. The mechanism concerning the absence of DNA-PKcs in M059J is due to the frameshift mutation in PRKDC (DNA-PKcs gene); however, the reason for the low-expression of ATM in M059J cells remains unclear. We showed here that the main reason for the lower ATM level in M059J cells was not related to the transcriptional regulation or protein degradation but was related to post-transcriptional regulation. Based on database information, we found that the 3'-untranslational region (UTR) of ATM contains a miR-100 binding site. By using an RNase protection assay and qRT-PCR, we identified that miR-100 is highly-expressed in M059J cells. We further demonstrated that miR-100 bound to the 3'-UTR of ATM. Knocking down miR-100 promotes ATM expression in M059J cells. Up-regulating miR-100 in M059K cells and other cancer cells reduces ATM expression and sensitizes these cells to ionizing radiation. These results indicate that ATM is a target of miR-100, elucidating that the low-expression of ATM in M059J cells is mainly due to the high expression of miR-100. These results also suggest that miR-100 could be a useful tool to target ATM and sensitize tumor cells to ionizing radiation.
| S-EPMC2970684 | biostudies-literature
Project description:The effects of tanshinone IIA on the proliferation of the human non-small cell lung cancer cell line A549 and its possible mechanism on the VEGF/VEGFR signal pathway were investigated. The exploration of the interaction between tanshinone IIA and its target proteins provides a feasible platform for studying the anticancer mechanism of active components of herbs. The CCK-8 assay was used to evaluate the proliferative activity of A549 cells treated with tanshinone IIA (2.5-80 ?mol/L) for 24, 48 and 72 h, respectively. Flow cytometry was used for the detection of cell apoptosis and cell cycle perturbation. VEGF and VEGFR2 expression were studied by Western blotting. The binding mode of tanshinone IIA within the crystal structure of the VEGFR2 protein was evaluated with molecular docking analysis by use of the CDOCKER algorithm in Discovery Studio 2.1. The CCK-8 results showed that tanshinone IIA can significantly inhibit A549 cell proliferation in a dose- and time-dependent manner. Flow cytometry results showed that the apoptosis rate of tested group was higher than the vehicle control, and tanshinone IIA-treated cells accumulated at the S phase, which was higher than the vehicle control. Furthermore, the expression of VEGF and VEGFR2 was decreased in Western blot. Finally, molecular docking analysis revealed that tanshinone IIA could be stably docked into the kinase domain of VEGFR2 protein with its unique modes to form H-bonds with Cys917 and ?-? stacking interactions with Val848. In conclusion, tanshinone IIA may suppress A549 proliferation, induce apoptosis and cell cycle arrest at the S phase. This drug may suppress angiogenesis by targeting the protein kinase domains of VEGF/VEGFR2.
| S-EPMC4675810 | biostudies-literature