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The role of Foxp1/4 in lung development

ABSTRACT: Foxp1/4 transcription factors are conserved transcriptional repressors expressed in overlapping patterns during lung development as well as in the adult lung. However, the role of Foxp1/4 in development and homeostasis of the pseudostratified epithelium of the proximal airways and trachea is unknown. We propose to determine the roles for Foxp1/4 in lung development by deleting these genes in lung epithelial specific knockout mice. To explore the genome wide consequences of Foxp1/4 deficiency on secretory epithelial differentiation in the lung, we performed microarray analysis of Shh- cre control and Foxp1/4ShhcreDKO mutants lungs at E14.5, 3 embryos, respectively.

ORGANISM(S): Mus musculus

SUBMITTER: Shanru Li

PROVIDER: E-GEOD-34584 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Foxp1/4 control epithelial cell fate during lung development and regeneration through regulation of anterior gradient 2.

Li Shanru S Wang Yi Y Zhang Yuzhen Y Lu Min Min MM DeMayo Francesco J FJ Dekker Joseph D JD Tucker Philip W PW Morrisey Edward E EE

Development (Cambridge, England) 20120606 14

The molecular pathways regulating cell lineage determination and regeneration in epithelial tissues are poorly understood. The secretory epithelium of the lung is required for production of mucus to help protect the lung against environmental insults, including pathogens and pollution, that can lead to debilitating diseases such as asthma and chronic obstructive pulmonary disease. We show that the transcription factors Foxp1 and Foxp4 act cooperatively to regulate lung secretory epithelial cell ...[more]

PMID: 22675208

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The role of Foxp1/4 in lung development

Project description:Foxp1/4 transcription factors are conserved transcriptional repressors expressed in overlapping patterns during lung development as well as in the adult lung. However, the role of Foxp1/4 in development and homeostasis of the pseudostratified epithelium of the proximal airways and trachea is unknown. We propose to determine the roles for Foxp1/4 in lung development by deleting these genes in lung epithelial specific knockout mice.

2012-08-02 | GSE34584 | GEO

Knockdown of FOXP1 promotes the development of lung adenocarcinoma

Project description:Lung cancer is one of the most common cancers in the world, which accounts for about 27% of all cancer deaths. However, the mechanisms underlying the pathogenesis of lung cancer cells remain largely elusive. In this study, we examined the role of the Forkhead box protein P1 (FOXP1) in lung cancer development. Our Oncomine analysis shows that FOXP1 is downregulated in lung adenocarcinoma compared with normal lung tissue. Knockdown of FOXP1 promotes the proliferation growth and invasion of PC9 and A549 cells by regulating genes of chemokine signaling molecules, including CCR1, ADCY5, GNG7, VAV3, and PLCB1. Simultaneous knockdown of CCR1 and FOXP1 attenuated FOXP1 knockdown-induced increase of lung cancer cell growth. Finally, knockdown of FOXP1 in PC9 cells promotes the tumorigenesis via CCR1 signaling in xenograft mouse model. Taken together, our data suggest that FOXP1 plays important roles in preventing lung adenocarcinoma development via suppressing chemokine signaling pathways. Novel strategies might be developed to prevent the development of lung adenocarcinoma by targeting FOXP1

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The role of Foxp1/2/4 in lung endoderm identity

Project description:Our previous work has demonstrated an important role for the Foxp1/2/4 subfamily of transcriptional repressors in promoting lung epithelial differentiation. However, the overall role of this transcription factor subfamily in early lung endoderm identity is unknown.

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Knockdown of FOXP1 promotes the development of lung adenocarcinoma

Project description:Knockdown of FOXP1 promotes the development of lung adenocarcinoma

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Expression data from Ezh2 epithelial knock-out mouse lungs at E14.5

Project description:Ezh2 epigenetically suppresses developmentally-regulated genes. Ezh2 is highly expressed during development, including in the lung. We knocked out Ezh2 in the developing lung epithelium using a Shh-cre driver which is active in foregut endoderm prior to lung morphogenesis. Many developmentally regulated genes became derepressed in the mutant lungs, leading to defects in lung development. Microarray analysis of genes upregulated in Ezh2 epithelial knock-out mouse lungs compared to Shh-cre controls. We generated Ezh2 epithelial mutant lungs by crossing the Ezh2-floxed line (Su et al., 2003) with the Shh-cre line (Harfe et al., 2004). We isolated RNA from whole mouse lungs at embryonic day 14.5 from 4 Shh-cre:Ezh2-flox/flox embryos (M1-M4) and 4 Shh-cre embryos (C1-C4). Littermates are as follows: C1+C2; C3+C4; M1+M2; M3+M4.

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Role of Fzd2 in lung epithelium development

Project description:Fzd2 is a Wnt receptor expressed in the embryonic lung. We made a conditional knockout of Fzd2 to specifically address the role of signaling through Fzd2 in lung epithelial development. To explore the genes that are regulated by signaling through the Fzd2 receptor in the lung epithelium, we performed microarray analysis of Shhcre control and Fzd2CKO lungs at E12.5

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Human nasopharyngeal cancer cell HONE1 FOXP1 immunoprecipitates LC-MS

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Gene expression changes in stimulated and unstimulated Foxp1-deficient B cells.

Project description:Foxp1 is expressed throughout B cell development, but the physiological functions in mature B lymphocytes are unknown. We therefore evaluated differential gene expression in Foxp1-deficient B cells, with or withouth IgM stimulation.

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Non-IG Aberrations of FOXP1 in B-Cell Malignancies Lead to an Aberrant Expression of N-Truncated Isoforms of FOXP1

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