Homo sapiens
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: E-GEOD-39121
PROVIDER: PRJNA170053 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR518622.fastq.gz | Fastqsanger.gz | |||
| SRR518623.fastq.gz | Fastqsanger.gz | |||
| SRR518624.fastq.gz | Fastqsanger.gz | |||
| SRR518625.fastq.gz | Fastqsanger.gz | |||
| SRR518626.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 6 |
Similar Datasets
Project description:Molecular programs that mediate normal cell differentiation are required for oncogenesis and tumor cell survival in certain types of cancers. How cell lineage restricted genes specifically influence metastatic progression is poorly defined. In lung cancers, we uncovered an alveolar cell-selective transcriptional program that preferentially correlates with lung adenocarcinoma metastasis. This program is required for epithelial specification in the distal airways and is partially regulated by the lineage transcription factors GATA6 and HOPX. These factors cooperatively restrain the metastatic competence of adenocarcinoma cells, without affecting their survival, through the modulation of alveologenic and invasogenic target genes. Thus, GATA6 and HOPX are critical nodes in a lineage-selective pathway that directly links alveolar cell fate with metastasis suppresion in the lung adenocarcinoma subtype. mRNA profiles of human lung Adenocarcinoma PC9 cell lines infected with lentivirus harboring shRNA of control (Arab1) and shRNA of both GATA6 and HOPX were generated by deep sequencing, in triplicate, using Illumina HiSeq2000.
2013-06-10 | E-GEOD-39121 | biostudies-arrayexpress
Project description:Lung adenocarcinoma metastasis is suppressed by the alveolar lineage transcription factors GATA6 and HOPX.
2019-05-14 | E-GEOD-39121 | ExpressionAtlas
Project description:Molecular programs that mediate normal cell differentiation are required for oncogenesis and tumor cell survival in certain cancers. How cell-lineage-restricted genes specifically influence metastasis is poorly defined. In lung cancers, we uncovered a transcriptional program that is preferentially associated with distal airway epithelial differentiation and lung adenocarcinoma (ADC) progression. This program is regulated in part by the lineage transcription factors GATA6 and HOPX. These factors can cooperatively limit the metastatic competence of ADC cells, by modulating overlapping alveolar differentiation and invasogenic target genes. Thus, GATA6 and HOPX are critical nodes in a lineage-selective pathway that directly links effectors of airway epithelial specification to the inhibition of metastasis in the lung ADC subtype.
2013-06-10 | GSE39121 | GEO
Project description:LKB1 is among the most frequently altered tumor suppressors in lung adenocarcinoma. Inactivation of Lkb1 accelerates the growth and progression of oncogenic KRAS-driven lung tumors in mouse models. However, the molecular mechanisms by which LKB1 constrains lung tumorigenesis and whether the aggressive cancer state that stems from Lkb1 deficiency can be reverted remains unknown. To identify the processes governed by LKB1 in vivo, we generated an allele which enables Lkb1 inactivation during tumor development and subsequent Lkb1 restoration in established tumors. Restoration of Lkb1 in oncogenic KRAS-driven lung tumors suppressed proliferation and promoted tumor stasis. Lkb1 restoration activated targets of C/EBP transcription factors and drove the transition of neoplastic cells from a progenitor-like state to a less proliferative alveolar type II cell-like state. We show that C/EBP transcription factors govern a subset of genes that are induced by LKB1 and depend upon NKX2-1. We also demonstrate that a defining factor of the alveolar type II lineage, C/EBPα, constrains oncogenic KRAS-driven lung tumor growth. Thus, we uncover a role for a critical tumor suppressor in the regulation of key lineage-specific transcription factors, thereby constraining lung tumor development through the enforcement of differentiation.
2021-12-23 | PXD026738 | Pride
Project description:Lineage selective transcription factors (TFs) are important regulators of tumorigenesis, but their biological functions are often context dependent and their epigenetic mechanisms of action undefined. In this study, we uncover a conditional role for the endodermal and pulmonary specifying TF GATA6 during the initiation and progression of Kras mutant lung adenocarcinoma (LUAD). Inhibition of Gata6 in genetically engineered mouse models dampens the proliferation and increases the differentiation of LUAD tumors. These effects are influenced in part by the epithelial cell type that is targeted for transformation. In lung cancer cells derived from surfactant protein C expressing progenitors, we identify multiple genomic loci that are bound by GATA6. Moreover, suppression of Gata6 in these cells significantly alters chromatin accessibility, particularly at distal enhancer elements. Analogous to its paradoxical activity in the developing lungs, GATA6 expression fluctuates during different stages of LUAD progression and can control diverse lineage gene expression networks associated with cell proliferation, alveolar specification, BMP signaling, and epithelial plasticity. These findings demonstrate how GATA6 can broadly modulate the epigenome of lung tumor cells, which in turn may potentiate its divergent functions during cancer progression
2020-03-05 | GSE124602 | GEO
Project description:Lineage selective transcription factors (TFs) are important regulators of tumorigenesis, but their biological functions are often context dependent and their epigenetic mechanisms of action undefined. In this study, we uncover a conditional role for the endodermal and pulmonary specifying TF GATA6 during the initiation and progression of Kras mutant lung adenocarcinoma (LUAD). Inhibition of Gata6 in genetically engineered mouse models dampens the proliferation and increases the differentiation of LUAD tumors. These effects are influenced in part by the epithelial cell type that is targeted for transformation. In lung cancer cells derived from surfactant protein C expressing progenitors, we identify multiple genomic loci that are bound by GATA6. Moreover, suppression of Gata6 in these cells significantly alters chromatin accessibility, particularly at distal enhancer elements. Analogous to its paradoxical activity in the developing lungs, GATA6 expression fluctuates during different stages of LUAD progression and can control diverse lineage gene expression networks associated with cell proliferation, alveolar specification, BMP signaling, and epithelial plasticity. These findings demonstrate how GATA6 can broadly modulate the epigenome of lung tumor cells, which in turn may potentiate its divergent functions during cancer progression
2020-03-05 | GSE124601 | GEO
Project description:Lineage selective transcription factors (TFs) are important regulators of tumorigenesis, but their biological functions are often context dependent and their epigenetic mechanisms of action undefined. In this study, we uncover a conditional role for the endodermal and pulmonary specifying TF GATA6 during the initiation and progression of Kras mutant lung adenocarcinoma (LUAD). Inhibition of Gata6 in genetically engineered mouse models dampens the proliferation and increases the differentiation of LUAD tumors. These effects are influenced in part by the epithelial cell type that is targeted for transformation. In lung cancer cells derived from surfactant protein C expressing progenitors, we identify multiple genomic loci that are bound by GATA6. Moreover, suppression of Gata6 in these cells significantly alters chromatin accessibility, particularly at distal enhancer elements. Analogous to its paradoxical activity in the developing lungs, GATA6 expression fluctuates during different stages of LUAD progression and can control diverse lineage gene expression networks associated with cell proliferation, alveolar specification, BMP signaling, and epithelial plasticity. These findings demonstrate how GATA6 can broadly modulate the epigenome of lung tumor cells, which in turn may potentiate its divergent functions during cancer progression
2020-03-05 | GSE124603 | GEO
Project description:Hopx is a transcription co-factor expressed during lung development and we wanted to profile Hopx +/+ and -/- embyonic lungs. Results inform the role of Hopx in embryonic lung development We used microarrays to profile the transcriptome of Hopx -/- lungs compared to Hopx +/+ lungs. Lungs were microdissected and three biological replicates were used for each genotype.
2015-02-10 | E-GEOD-65755 | biostudies-arrayexpress
Project description:Hopx is a transcription co-factor expressed during lung development and we wanted to profile Hopx +/+ and -/- embyonic lungs. Results inform the role of Hopx in embryonic lung development
2015-02-10 | GSE65755 | GEO
Project description:PPARGC1A oppositely regulates cancer metastasis in melanoma, breast, and pancreatic cancer; however, little is known about its impact on lung cancer metastasis. We generated gene-expression profile of control and PPARGC1A suppressed A549 cells, a lung adenocarcinoma cell line that expresses moderate levels of PPARGC1A to investigate the role of this gene in lung cancer metastasis.
2021-08-16 | GSE156833 | GEO