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E-GEOD-39121

ABSTRACT: Lung adenocarcinoma metastasis is suppressed by the alveolar lineage transcription factors GATA6 and HOPX.

OTHER RELATED OMICS DATASETS IN: PRJNA170053

PROVIDER: E-GEOD-39121 | ExpressionAtlas | 2019-05-14

REPOSITORIES: ExpressionAtlas

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			Action	DRS
	E-GEOD-39121-analysis-methods.tsv	Tabular
	E-GEOD-39121-analytics.tsv	Tabular
	E-GEOD-39121-analytics.tsv.undecorated	Tabular
	E-GEOD-39121-analytics.tsv.undecorated.unrounded	Tabular
	E-GEOD-39121-analytics.tsv.unrounded	Tabular

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Project description:Lung adenocarcinoma metastasis is suppressed by the alveolar lineage transcription factors GATA6 and HOPX.

| PRJNA170053 | ENA

Lung adenocarcinoma metastasis is suppressed by the alveolar lineage transcription factors GATA6 and HOPX.

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

LKB1 drives stasis and C/EBP-mediated reprogramming to an alveolar type II fate in lung cancer

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

Lung adenocarcinoma metastasis is suppressed by the alveolar lineage transcription factors GATA6 and HOPX.

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

mRNA expression profiling A549 lung cancer cells following PPARGC1A suppression

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.

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H3K9 methyltransferases and demethylases control lung tumor-propagating cells and lung cancer progression

Project description:We have identified the histone methyltransferases G9a/Glp as suppressors of aggressive lung tumor-propagating cells (TPCs). Chemically inhibiting G9a/Glp promoted TPC phenotypes in lung adenocarcinoma cells, and caused chromatin changes at genes associated with the differentiation of stem cells. G9a/Glp inhibition in lung progenitor cell organoid cultures disrupted alveolar differentiation. Depleting G9a during tumorigenesis enriched for TPCs, accelerating disease progression and metastasis. Demethylase inhibition decreased lung adenocarcinoma progression in vivo.

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H3K9 methyltransferases and demethylases control lung tumor-propagating cells and lung cancer progression (experiment 2)

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MTSS1 Suppresses NF-kB Activity in Lung Adenocarcinoma through Repression of RelA/p65 Phosphorylation

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The ETS transcription factor Elf5 drives lung metastasis in luminal breast cancer via recruitment of Gr-1+CD11b+ myeloid derived suppressor cells [acute]

Project description:Elf5 expression in mammary progenitor cells regulates a cell fate decision that establishes the alveolar cell lineage. In luminal breast cancer cells, increased Elf5 expression suppressed estrogen receptor and FoxA1 expression and was implicated in the acquisition of resistance to the cytostatic effects of antiestrogen therapy. We show that in the PyMT model of luminal breast cancer, increased Elf5 expression drives lung metastasis by recruiting myeloid-‐derived suppressor cells, and that this activity overcomes the epithelializing influence of Elf5. Breast cancer expression signatures identify a similar process in humans, and increased Elf5 immunohistochemical staining predicts poor prognosis in the luminal A subgroup. Thus Elf5 may promote escape from hormonal therapy and drive metastasis in luminal breast cancer.

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The ETS transcription factor Elf5 drives lung metastasis in luminal breast cancer via recruitment of Gr-1+CD11b+ myeloid derived suppressor cells [chronic]

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