Embelin induced differential gene expression in A549 lung cancer cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Avisetti DR
PROVIDER: S-ECPF-GEOD-50545 | biostudies-other | 2014
REPOSITORIES: biostudies-other
Similar Datasets
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.
2014-01-25 | E-GEOD-50545 | biostudies-arrayexpress
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)
2014-01-25 | GSE50545 | GEO
Project description:Toll-like receptor 10 (TLR10) is the only member of the TLR family whose function and ligand have not been clearly described. Literature reports on its function are contradictory and suggest a possible immunomodulatory role that depends on the cell type, the pathogen, and the level of TLR10 expression. To investigate the regulatory role of TLR10 in A549 lung epithelial cells, we overexpressed TLR10 using CRISPRa technology and examined the differential expression of various genes involved in TLR signaling activated by different TLR ligands, namely dsRNA, LPS, and Pam3Cys. The expression of proinflammatory cytokines, such as IL1β, IFNβ, TNFα, IL8, CXCL10, and CCL20, decreased in the challenged cells overexpressing TLR10, whereas the expression of the anti-inflammatory cytokine IL10 and the antimicrobial peptide hβD-2 increased. For several of the regulated inflammatory markers, we were able to show the change in gene expression was translated to the protein level. It appears that TLR10 can function as an anti-inflammatory in A549 cells, depending on its expression level and that the mode of action may be virulence factor-specific. The potential suppression of inflammation by regulating expression of TLR10 in lung epithelial cells may allow the development of new approaches to balance an inflammatory response and prevent extensive tissue damage in respiratory diseases.
| S-EPMC9855645 | biostudies-literature
Project description:While anaesthetics are frequently used on cancer patients during surgical procedures, their consequence on cancer progression remains to be elucidated. In this study, we sought to investigate the influence of local anesthetics on lung cancer cell dissemination in vitro and in vivo. A549 human non-small lung cancer cells were treated with various local anaesthetics including ropivacaine, lidocaine, levobupivacaine and bupivacaine. Cell barrier property was assessed using an electric cell-substrate impedance sensing (ECIS) system. The epithelial-to-mesenchymal transition (EMT) of treated cells was studied by immunofluorescence staining. In vitro and in vivo cancer cell dissemination were investigated.Gene expression microarray and quantitative real-time PCR (qrt-PCR) assays were used to identify the genes responsible for levobupivacaine-mediated cancer cell dissemination.The results illustrated that only levobupivacaine induced EMT in the treated cells and also caused the dissemination of cancer cells in vitro. In addition, after intravenous injection, levobupivacaine encouraged cancer cell dissemination in vivo. Gene expression microarray, qrt-PCR and immunoblotting revealed that after levobupivacaine treatment, the hypoxia-inducible factor (HIF)- 2? gene was upregulated in cancer cells. Our findings suggest that levobupivacaine may induce A549 lung cancer cell dissemination both in vitro and in vivo. More specifically, HIF-2? signaling possibly contributes to levobupivacaine-mediated A549 lung cancer cell dissemination.
| S-EPMC5561232 | 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:Arsenic is methylated during its metabolism, thereby depleting the intracellular methyl donor S-adenosyl-methionine, which may lead to disturbances in DNA methylation patterns which could lead to altered gene expression Cells were exposed to sodium arsenite (NaAsO2, Sigma) at concentrations of 0.08 µM, 0.4 µM and 2 µM for 1, 2 and 8 weeks.
| S-ECPF-GEOD-44169 | biostudies-other
Project description:Endometrial cancer (EMCA) is a clinically heterogeneous disease. Previously, we tested the efficacy of Verteporfin (VP) in EMCA cells and observed cytotoxic and anti-proliferative effects. In this study, we analyzed RNA sequencing data to investigate the comprehensive transcriptomic landscape of VP treated Type 1 EMCA cell lines, including HEC-1-A and HEC-1-B. There were 549 genes with differential expression of two-fold or greater and P?<?0.05 after false discovery rate correction for the HEC-1-B cell line. Positive regulation of TGF?1 production, regulation of lipoprotein metabolic process, cell adhesion, endodermal cell differentiation, formation and development, and integrin mediated signaling pathway were among the significantly associated terms. A functional enrichment analysis of differentially expressed genes after VP treatment revealed extracellular matrix organization Gene Ontology as the most significant. CDC23 and BUB1B, two genes crucially involved in mitotic checkpoint progression, were found to be the pair with the best association from STRING among differentially expressed genes in VP treated HEC-1-B cells. Our in vivo results indicate that subcutaneous tumors in mice were regressed after VP treatment by inhibiting cell cycle pathway proteins. The present study revealed multiple key genes of pathological significance in EMCA, thereby improving our understanding of molecular profiles of EMCA cells.
| S-EPMC6405995 | biostudies-literature
Project description:BackgroundRecent technological advances in atmospheric plasmas have made the creation of non-thermal atmospheric pressure plasma (NTP) possible for utilization in the medical field. Although accumulated evidence suggests that NTP induces cell death in various cancer cell types thus offering a promising alternative treatment strategy, the mechanism underlying its therapeutic effect is not fully understood.ResultsWe analyzed relevant signaling cascades associated with the tumor protein p53, in particular the cell cycle arrest, DNA damage as well as the underlying apoptosis pathways. Based on our results, the major effect from plasma exposure was found to be the activation of MAPK and p53 signaling pathways, resulting in changes in gene expression of MEKK, GADD, FOS and JUN. Finally, a significant modulation in expression of genes related to cellular proliferation and differentiation was observed.ConclusionOverall, the presented data of the tumor transcriptome helped identify the key players in modulated gene expression following exposure to plasma at the molecular level, and also helped interpret the downstream processes. The present work laid the foundation for further studies to clarify the roles of multiple pathways in plasma-induced biological processes. Further investigation of these genes in other cell lines may reveal comprehensive mechanisms of plasma induced effects.
| S-EPMC4483225 | biostudies-literature
Project description:Because of similarities in histopathology and tumor progression stages between mouse and human lung adenocarcinomas, the mouse lung tumor model with lung adenomas as the endpoint has been used extensively to evaluate the efficacy of putative lung cancer chemopreventive agents. In this study, a competitive cDNA library screening (CCLS) was employed to determine changes in the expression of mRNA in chemically induced lung adenomas compared with paired normal lung tissues. A total of 2555 clones having altered expression in tumors were observed following competitive hybridization between normal lung and lung adenomas after primary screening of over 160,000 clones from a mouse lung cDNA library. Among the 755 clones confirmed by dot blot hybridization, 240 clones were underexpressed, whereas 515 clones were overexpressed in tumors. Sixty-five clones with the most frequently altered expression in six individual tumors were confirmed by semiquantitative RT-PCR. When examining the 58 known genes, 39 clones had increased expression and 19 had decreased expression, whereas the 7 novel genes showed overexpression. A high percentage (>60%) of overexpressed or underexpressed genes was observed in at least two or three of the lesions. Reproducibly overexpressed genes included ERK-1, JAK-1, surfactant proteins A, B, and C, NFAT1, alpha-1 protease inhibitor, helix-loop-helix ubiquitous kinase (CHUK), alpha-adaptin, alpha-1 PI2, thioether S-methyltransferase, and CYP2C40. Reproducibly underexpressed genes included paroxanase, ALDH II, CC10, von Ebner salivary gland protein, and alpha- and beta-globin. In addition, CCLS identified several novel genes or genes not previously associated with lung carcinogenesis, including a hypothetical protein (FLJ11240) and a guanine nucleotide exchange factor homologue. This study shows the efficacy of this methodology for identifying genes with altered expression. These genes may prove to be helpful in our understanding of the genetic basis of lung carcinogenesis and in developing biomarkers for lung cancer chemoprevention studies in mice.
| S-EPMC1502122 | biostudies-literature
Project description:The tumor microenvironment plays an important role in regulating cell growth and metastasis. Recently, we developed an ex vivo lung cancer model (four dimensional, 4D) that forms perfusable tumor nodules on a lung matrix that mimics human lung cancer histopathology and protease secretion pattern. We compared the gene expression profile (Human OneArray v5 chip) of A549 cells, a human lung cancer cell line, grown in a petri dish (two-dimensional, 2D), and of the same cells grown in the matrix of our ex vivo model (4D). Furthermore, we obtained gene expression data of A549 cells grown in a petri dish (2D) and matrigel (three-dimensional, 3D) from a previous study and compared the 3D expression profile with that of 4D. Expression array analysis showed 2,954 genes differentially expressed between 2D and 4D. Gene ontology (GO) analysis showed upregulation of several genes associated with extracellular matrix, polarity and cell fate and development. Moreover, expression array analysis of 2D vs. 3D showed 1,006 genes that were most differentially expressed, with only 36 genes (4%) having similar expression patterns as observed between 2D and 4D. Finally, the differential gene expression signature of 4D cells (vs. 2D) correlated significantly with poor survival in patients with lung cancer (n = 1,492), while the expression signature of 3D vs. 2D correlated with better survival in lung cancer patients with lung cancer. As patients with larger tumors have a worse rate of survival, the ex vivo 4D model may be a good mimic of natural progression of tumor growth in lung cancer patients.
| S-EPMC4070715 | biostudies-literature