Ontology highlight
ABSTRACT:
PROVIDER: PRJNA916295 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR22904085.fastq.gz | Fastqsanger.gz | |||
| SRR22904086.fastq.gz | Fastqsanger.gz | |||
| SRR22904087.fastq.gz | Fastqsanger.gz | |||
| SRR22904088.fastq.gz | Fastqsanger.gz | |||
| SRR22904089.fastq.gz | Fastqsanger.gz |
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Project description:Exposure to genotoxic stress promotes cell-cycle arrest and DNA repair or apoptosis. These “life” or “death” cell fate decisions often rely on the activity of the tumor suppressor gene p53. Therefore, how p53 activity is precisely regulated is essential to maintain tissue homeostasis and to prevent cancer development. Here we demonstrate that Drosophila p53 pro-apoptotic activity is regulated by the G2/M kinase Cdk1. We find that cell cycle arrested or endocycle-induced cells are refractory to ionizing radiation induced apoptosis. We show that the p53 protein is not able to bind to the p53 responding elements of the pro-apoptotic genes and to activate their expression in experimentally arrested cells. Our results indicate that p53 genetically and physically interacts with Cdk1 and that p53 pro-apoptotic role is regulated by the cell cycle status of the cell. We propose a model in which cell cycle progression and p53 pro-apoptotic activity are molecularly connected to coordinate the appropriate response after DNA damage.
2021-11-26 | GSE169668 | GEO
Project description:Hepatocellular carcinoma is one of the most common cancers in world wide. During tumorigenesis, tumor suppressor and cancer-related genes are commonly silenced by aberrant DNA methylation in their promoter regions. Zebularine [1-(β-ᴅ-ribofuranosyl)-1,2-dihydropyrimidin-2-one] acts as an inhibitor of DNA methylation and exhibits chemical stability and minimal cytotoxicity both in vitro and in vivo. In this study, we explore the effect and possible mechanism of action of zebularine on hepatocellular carcinoma cell line HepG2. Here, we demonstrated that zebularine exhibited antitumor activity on HepG2 cells by inhibiting cell proliferation and inducing apoptosis. Zebularine treatment down-regulated CDK2 and phosphorylation of retinoblastoma protein (RB), and up-regulated p21WAF/CIP1 and p53. We also found that zebularine treatment up-regulated phosphorylation of p44/42 MAPK. These results suggest that p44/42 MAPK pathway play a role in zebularine induced cell cycle arrest by regulating activity of p21WAF/CIP1 and Rb. Furthermore, we found that zebularine induced apoptosis. Although proapoptotic protein Bax levels were not affected, antiapoptotic protein Bcl-2 level was down-regulated with zebularine treatment. The data in the present study suggest that the action of the double-stranded RNA-dependent protein kinase (PKR) is involved in inducing apoptosis with zebularine. These results provide a novel mechanism of zebularine-induced cell growth arrest and apoptosis in hepatocellular carcinoma. Three each independent batches of zebuluarine-treated and control HepG2 cells were subjected to illumina Human methylation 450K Beadchip analysis.
2013-12-01 | E-GEOD-42490 | biostudies-arrayexpress
Project description:Rhodacyanine, a series of cyanines derived from rhodanine, exerts anticancer effects. This study intended to uncover the biological mechanism underlying the anticancer effects of a a fluorinated rhodacyanine in HeLa cervical cancer cells. Initially, the cytotoxic activities of 15 compounds were screened, Rho-7 exhibited the most effective compound against Hela cell growth with IC50 values at 0.03 µM. Interestingly, Rho-7-targeted mitochondrial damage leads to cancer cell death by increasing reactive oxygen species (ROS) levels. Additionally, Rho-7 can trigger Hela cells to undergo apoptosis and cell cycle arrest at the G2/M phase. Rho-7 could downregulate the expression of anti-apoptotic Mcl-1 genes or upregulate the level of pro-apoptotic Bad and Bik genes. Our findings suggest that the anticancer activity of Rho-7 involve ROS generation, cell cycle arrest and apoptotic induction, as well as alteration of pro-and anti-apoptotic genes, displaying a therapeutic potential of Rho-7 in cervical cancer treatment.
2024-01-01 | GSE251969 | GEO
Project description:Aspongopus chinensis (Coridius chinensis) Genome sequencing and assembly
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Project description:Histone deacetylase (HDAC) inhibition has been shown in previous studies to disrupt the synovial sarcoma oncoprotein complex, resulting in apoptosis. To understand the molecular effects of HDAC inhibition, RNA-Seq transcriptome analysis was undertaken in six human synovial sarcoma cell lines. HDAC inhibition induced pathways of cell cycle arrest, neuronal differentiation and response to oxygen-containing species, effects also observed in other cancers treated with this class of drugs. More specific to synovial sarcoma, polycomb-group targets were reactivated including tumor suppressor CDKN2A, and pro-apoptotic transcriptional patterns were induced. Functional analyses revealed that ROS-mediated FOXO activation and pro-apoptotic factors BIK, BIM and BMF were important to apoptosis induction following HDAC-inhibition in synovial sarcoma
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Project description:The p53 protein is a cell-autonomous tumor suppressor that restricts malignant transformation by triggering cell cycle exit or apoptosis. p53 also promotes cellular senescence, a program that triggers a stable cell cycle arrest and can modify the tissue microenvironment through its effect on cell membrane and secretory proteins. Here we show that specific ablation of p53 in hepatic stellate cells, which undergo a process of proliferation and senescence in the fibrogenic response to liver damage, enhances liver cirrhosis, reduces survival and increases the malignant transformation of adjacent epithelial cells into hepatocellular carcinoma. This p53-dependent senescence program involves the release of secreted proteins which skew macrophages into a tumor-inhibiting M1-state that can eliminate senescent stellate cells. In contrast, p53-deficient stellate cells secrete factors that promote M2 polarization, which is pro-tumorigenic. Our study reveals that p53 can exert a non-cell-autonomous tumor suppressor response and suggests that this occurs, in part, by its ability to influence macrophage polarization. We used microarrays to detail the global programme of gene expression underlying p53-dependent senescent and identified distinct classes of up-regulated or down-regulated genes during this process. Proliferating and senescent stellate cell pellets were collected RNA extraction and hybridization on Affymetrix microarrays.
2013-04-05 | E-GEOD-39469 | biostudies-arrayexpress
Project description:Hepatocellular carcinoma is one of the most common cancers in world wide. During tumorigenesis, tumor suppressor and cancer-related genes are commonly silenced by aberrant DNA methylation in their promoter regions. Zebularine [1-(β-ᴅ-ribofuranosyl)-1,2-dihydropyrimidin-2-one] acts as an inhibitor of DNA methylation and exhibits chemical stability and minimal cytotoxicity both in vitro and in vivo. In this study, we explore the effect and possible mechanism of action of zebularine on hepatocellular carcinoma cell line HepG2. Here, we demonstrated that zebularine exhibited antitumor activity on HepG2 cells by inhibiting cell proliferation and inducing apoptosis. Zebularine treatment down-regulated CDK2 and phosphorylation of retinoblastoma protein (RB), and up-regulated p21WAF/CIP1 and p53. We also found that zebularine treatment up-regulated phosphorylation of p44/42 MAPK. These results suggest that p44/42 MAPK pathway play a role in zebularine induced cell cycle arrest by regulating activity of p21WAF/CIP1 and Rb. Furthermore, we found that zebularine induced apoptosis. Although proapoptotic protein Bax levels were not affected, antiapoptotic protein Bcl-2 level was down-regulated with zebularine treatment. The data in the present study suggest that the action of the double-stranded RNA-dependent protein kinase (PKR) is involved in inducing apoptosis with zebularine. These results provide a novel mechanism of zebularine-induced cell growth arrest and apoptosis in hepatocellular carcinoma.
2013-12-01 | GSE42490 | GEO
Project description:Expression and differential expression analysis of custom probes for genomic regions that have been found to be differentially expressed (i) throughout cell cycle progression, (ii) in response to the anti-proliferative and pro-apoptotic p53 pathway, and (iii) the anti-apoptotic and pro-proliferative STAT-3 pathway. In addition, the Agilent custom array (244K) interrogates probes for genomic regions predicted to contain a conserved secondary structure identified by RNAz (Washietl et al. "Fast and reliable prediction of noncoding RNAs." Proc Natl Acad Sci USA. 102:2454-9, 2005.) or Evofold (Pedersen et al. "Identification and classification of conserved RNA secondary structures in the human genome." PLoS Comput Biol. 2:e33, 2006.), as well as known non-coding RNAs from public databases, and the Agilent mRNA probe sets 014850. Colorectal carcinoma cells with defunct TP53 compared to colorectal carcinoma cells with induced TP53. We analyzed three arrays each for colorectal carcinoma cells with defunct TP53 and with induced TP53 expression
2014-02-04 | E-GEOD-29794 | biostudies-arrayexpress