Gene expression profiling of A549 cells that undergo cell death
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Kang Ho Sung
PROVIDER: S-ECPF-GEOD-24271 | biostudies-other |
REPOSITORIES: biostudies-other
Similar Datasets
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).
2013-09-16 | GSE24271 | GEO
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.
2013-09-16 | E-GEOD-24271 | biostudies-arrayexpress
Project description:BACKGROUND: The 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. RESULTS: We 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. CONCLUSION: This 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: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:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series
| S-ECPF-GEOD-43494 | biostudies-other
Project description:Despite a distinct developmental origin, extraembryonic cells in mice contribute to gut endoderm and converge to transcriptionally resemble their embryonic counterparts. Notably, extraembryonic progenitors share a non-canonical epigenome, raising several pertinent questions, including whether this landscape is reset to match the embryonic regulation and if these cells persist into later development. Here, we developed a two-color lineage tracing strategy to track and isolate extraembryonic cells over time. We find that extraembryonic gut cells display substantial memory of their developmental origin including retention of their original DNA methylation landscape and resulting transcriptional signatures. Furthermore, we show that extraembryonic gut cells undergo programmed cell death and neighboring embryonic cells clear their remnants via non-professional phagocytosis. By midgestation, we no longer detect extraembryonic cells in the wild type gut while they persist and differentiate further in p53 mutant embryos. Our study provides key insights into the molecular and developmental fate of extraembryonic cells inside the embryo.
2024-04-04 | GSE250084 | GEO
Project description:To determine the signaling networks that are dysregulated in cisplatin-resistant non-small cell lung cancer, noncoding RNA expression data were obtained from, and compared between, the lung adenocarcinoma cell line, A549, and its cisplatin-resistant derivative, A549/CDDP. Noncoding RNA expression data from a cisplatin-sensitive lung adenocarcinoma cancer cell line (A549) were collected and compared to noncoding RNA expression data from a cisplatin-resistant cell line (A549/CDDP). 3 independent experiments were completed for both the sensitive and resistant cell lines.
| S-ECPF-GEOD-43249 | biostudies-other
Project description:We studied the effect of derrone (DR), one of the major compounds of unripe fruits of Cudrania tricuspidata, on cancer cell death. DR inhibited cell growth of various cancer cells, and that was partially associated with apoptosis in A549 cells. DR showed the autophagic features, such as the conversion of LC3-I to LC3-II, the formation of autophagosome and the downregulation of SQSTM1/p62 (p62). The treatment of autophagy inhibitor reversed DR-mediated cell death, suggesting that DR induces autophagic cell death. The increase of cytoplasmic Ca2+ and ROS by DR treatment significantly influences the formation of autophagosomes; however, only ROS scavengers significantly rescued the reduced cell viability. Additional results revealed that treatment of DR induces sustained phosphorylation of ERK and the inhibition of ERK phosphorylation using U0126 (ERK inhibitor) markedly attenuated DR-induced cell death. Overall, these results suggest that DR induces autophagic cell death through intracellular ROS and sustained ERK phosphorylation in A549 cells.
| S-EPMC6583947 | biostudies-literature
Project description:Despite a distinct developmental origin, extraembryonic cells in mice contribute to gut endoderm and converge to transcriptionally resemble their embryonic counterparts. Notably, extraembryonic progenitors share a non-canonical epigenome, raising several pertinent questions, including whether this landscape is reset to match the embryonic regulation and if these cells persist into later development. Here, we developed a two-color lineage tracing strategy to track and isolate extraembryonic cells over time. We find that extraembryonic gut cells display substantial memory of their developmental origin including retention of their original DNA methylation landscape and resulting transcriptional signatures. Furthermore, we show that extraembryonic gut cells undergo programmed cell death and neighboring embryonic cells clear their remnants via non-professional phagocytosis. By midgestation, we no longer detect extraembryonic cells in the wild type gut while they persist and differentiate further in p53 mutant embryos. Our study provides key insights into the molecular and developmental fate of extraembryonic cells inside the embryo.
2024-04-04 | GSE250181 | GEO
Project description:Despite a distinct developmental origin, extraembryonic cells in mice contribute to gut endoderm and converge to transcriptionally resemble their embryonic counterparts. Notably, extraembryonic progenitors share a non-canonical epigenome, raising several pertinent questions, including whether this landscape is reset to match the embryonic regulation and if these cells persist into later development. Here, we developed a two-color lineage tracing strategy to track and isolate extraembryonic cells over time. We find that extraembryonic gut cells display substantial memory of their developmental origin including retention of their original DNA methylation landscape and resulting transcriptional signatures. Furthermore, we show that extraembryonic gut cells undergo programmed cell death and neighboring embryonic cells clear their remnants via non-professional phagocytosis. By midgestation, we no longer detect extraembryonic cells in the wild type gut while they persist and differentiate further in p53 mutant embryos. Our study provides key insights into the molecular and developmental fate of extraembryonic cells inside the embryo.
2024-04-04 | GSE250180 | GEO