Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA314813 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR3214590.fastq.gz | Fastqsanger.gz | |||
| SRR3214581.fastq.gz | Fastqsanger.gz | |||
| SRR3214591.fastq.gz | Fastqsanger.gz | |||
| SRR3214582.fastq.gz | Fastqsanger.gz | |||
| SRR3214592.fastq.gz | Fastqsanger.gz |
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Project description:We report the gene expression profiles by NGFR knockdown in H460 and H1299 cell lines and reveal that NGFR ablation activates p53 target gene expression. We examined gene expression in two different non-small-cell lung cancer cell lines, one with wild-type p53 and the other without p53.
2016-06-10 | E-GEOD-79051 | biostudies-arrayexpress
Project description:We report the gene expression profiles by NGFR knockdown in H460 and H1299 cell lines and reveal that NGFR ablation activates p53 target gene expression.
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Project description:Secreted extracellular vesicles are known to influence the tumor microenvironment and promote metastasis. In this work, we have analyzed the involvement of extracellular vesicles in the establishment of lymph node pre-metastatic niches by melanoma cells. We found that small extracellular vesicles (sEVs) derived from highly metastatic melanoma cell lines spread broadly through the lymphatic system and were taken up by lymphatic endothelial cells, reinforcing lymph node metastasis. Melanoma-derived sEVs induce lymphangiogenesis, a hallmark of pre-metastatic niche formation, in vitro and in lymphoreporter mice in vivo. We found that neural growth factor receptor (NGFR) is secreted in melanoma-derived small extracellular vesicles and shuttled to lymphatic endothelial cells, inducing lymphangiogenesis and tumor cell adhesion through the activation of ERK and NF-B pathways and ICAM1 expression. Importantly, ablation or inhibition of NGFR in sEVs reversed the lymphangiogenic phenotype, decreased melanoma lymph node metastasis and extended the survival. Importantly, analysis of NGFR expression in lymph node metastases and matched primary tumors shows that levels of MITF+NGFR+ lymph node metastatic cells are correlated with disease outcome. Our data support the idea that NGFR secreted in sEVs favors lymph node pre-metastatic niche formation and lymph node metastasis in melanoma
2021-08-05 | PXD024852 | Pride
Project description:Secreted extracellular vesicles are known to influence the tumor microenvironment and promote metastasis. In this work, we have analyzed the involvement of extracellular vesicles in establishing the lymph node pre-metastatic niche by melanoma cells. We found that small extracellular vesicles (sEVs) derived from highly metastatic melanoma cell lines spread broadly through the lymphatic system and are taken up by lymphatic endothelial cells reinforcing lymph node metastasis. Melanoma-derived sEVs induce lymphangiogenesis, a hallmark of pre-metastatic niche formation, in vitro and in lymphoreporter mice in vivo. Analysis of involved factors demonstrated that the neural growth factor receptor (NGFR) is secreted in melanoma-derived small extracellular vesicles and shuttled to lymphatic endothelial cells inducing lymphangiogenesis and tumor cell adhesion through the activation of ERK and NF-B pathways and ICAM1 expression. Importantly, ablation or inhibition of NGFR in sEVs reversed the lymphangiogenic phenotype, decreased melanoma lymph node metastasis and extended mice survival. Importantly, analysis of NGFR expression in lymph node metastases and matched primary tumors shows that levels of MITF+NGFR+ lymph node metastatic cells are correlated with disease outcome. Our data support that NGFR is secreted in sEVs favoring lymph node pre-metastatic niche formation and lymph node metastasis in melanoma.
2021-07-16 | PXD024108 | Pride
Project description:Unlike other EBV-associated human tumors, nearly 100% wild-type p53 gene is found in NPC, p53 protein is also frequently found to accumulate in NPC biopsies. However, the role of p53 in EBV-positive nasopharyngeal carcinoma is unclear. The expression profiles of mRNAs and miRNAs of EBV-positive NPC cells are unknown. To elucidate the function of p53 in EBV-positive NPC, we used the CRISPR-Cas9 gene editing system to p53 knockout C666-1 cells with Epstein-Barr virus and performed mRNA and miRNA sequencing in p53 KO C666-1 and their control cells. Gene Ontology (GO), KEGG and STRING analyses were implemented to identify significant functions, pathways of differentially expressed mRNAs. Through comparative analysis of p53-regulated genes from EBV-positive C666-1 cells and EBV-negative HONE2 cells with p53 target genes from 16 high throughput data sets, we found that the number of target genes and KEGG pathways downregulated by p53 in EBV-positive C666-1 cells were much less than in EBV-negative HONE2 cells, but “p53 signaling pathway” and related cell cycle arrest and apoptosis genes were significantly downregulated after knockout of p53 gene in C666-1 cells. To explore the effect of p53 on cell cycle and apoptosis, we established stable p53 C666-1-KO cell lines with stable expression of exogenous p53-WT and their control cell lines. Using the established cell lines, we observed that stable expression of p53 repressed cell proliferation, increased cell apoptosis and blocked G1/S phase progression. In conclusion, our results show that the accumulated p53 protein in EBV-positive C666-1 cells still has some tumour suppressor functions such as blocking cell-cycle progression and promoting apoptosis, but the ability of p53 to downregulate gene expression is inhibited.
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Project description:Unlike other EBV-associated human tumors, nearly 100% wild-type p53 gene is found in NPC, p53 protein is also frequently found to accumulate in NPC biopsies. However, the role of p53 in EBV-positive nasopharyngeal carcinoma is unclear. The expression profiles of mRNAs and miRNAs of EBV-positive NPC cells are unknown. To elucidate the function of p53 in EBV-positive NPC, we used the CRISPR-Cas9 gene editing system to p53 knockout C666-1 cells with Epstein-Barr virus and performed mRNA and miRNA sequencing in p53 KO C666-1 and their control cells. Gene Ontology (GO), KEGG and STRING analyses were implemented to identify significant functions, pathways of differentially expressed mRNAs. Through comparative analysis of p53-regulated genes from EBV-positive C666-1 cells and EBV-negative HONE2 cells with p53 target genes from 16 high throughput data sets, we found that the number of target genes and KEGG pathways downregulated by p53 in EBV-positive C666-1 cells were much less than in EBV-negative HONE2 cells, but “p53 signaling pathway” and related cell cycle arrest and apoptosis genes were significantly downregulated after knockout of p53 gene in C666-1 cells. To explore the effect of p53 on cell cycle and apoptosis, we established stable p53 C666-1-KO cell lines with stable expression of exogenous p53-WT and their control cell lines. Using the established cell lines, we observed that stable expression of p53 repressed cell proliferation, increased cell apoptosis and blocked G1/S phase progression. In conclusion, our results show that the accumulated p53 protein in EBV-positive C666-1 cells still has some tumour suppressor functions such as blocking cell-cycle progression and promoting apoptosis, but the ability of p53 to downregulate gene expression is inhibited.
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Project description:Lung cancer is one of the most common and fatal cancer worldwide. There are two major types of lung cancer, non-small cell lung cancer (NSCLC) and small cell lung cancer (SCLC). Recently, gefitinib, a small molecule, which target tyrosine kinase, has been regarded as the first-line treatment in NSCLC patients. However, several patients have been observed tumor recurrence and eventually developed progressive outcomes after target therapy. Thus, an effective therapeutic approach need to be explored. Here, we found that ectopically expressed ATP synthase on plasma membrane exhibited gefitinib-resistance properties in lung cancer cell lines. Furthermore, we unraveled that citreoviridin, an ectopic ATP synthase inhibitor, suppressed the abilities of both proliferation and colony formation in lung cancer cell lines. To elucidate the comprehensive mechanism regulated by citreoviridin, we performed microarray analysis. The results indicated that not only mRNAs but also long non-coding RNAs (lncRNAs) are involved in citreoviridin-treated cell death. One of the well-known lncRNAs, growth arrest-specific transcript (GAS5), was robustly upregulated after citreoviridin treatment. In order to investigate the upstream modulator of GAS5, we utilized chromatin immunoprecipitation (ChIP) assay and revealed that E2F transcription factor 1 (E2F1) could bind to the promoter of GAS5. Consistently, both microarray and qPCR data showed the expression level of E2F1 was negatively correlated to GAS5 after citreoviridin treatment. The evidence suggests that E2F1 might be a potential repressor of GAS5. Furthermore, combining microarray and Gene Set Enrichment Analysis (GSEA) analysis as well as qPCR demonstrated that p53 pathway was activated. To further realize the GAS5-p53 regulating network, RNA-protein pull-down assay followed by LC-MS/MS will be utilized to dissect the GAS5-interacting proteomic profiling.From the results, we identified 107 GAS5-interacting proteins in common from A549 and H1975 cell lines. Our proteomics experiments identified topoisomerase 2-alpha (TOP2A) as the key protein involved in the citreoviridin-regulated gefitinib-resistance pathway, therefore, we picked out TOP2A for further study. Additionally, we further validated the interaction between TOP2A and GAS5 by western blot and RNA immunoprecipitation (RIP). Taken together, this study suggests targeting E2F1/GAS5/p53 axis is a potential therapeutic strategy for gefitinib-resistant lung cancer.
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