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Knockdown of FOXP1 promotes the development of lung adenocarcinoma

ABSTRACT: Knockdown of FOXP1 promotes the development of lung adenocarcinoma

PROVIDER: PRJNA427471 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6417890_1.fastq.gz	Fastqsanger.gz
	SRR6417890_2.fastq.gz	Fastqsanger.gz
	SRR6417885_1.fastq.gz	Fastqsanger.gz
	SRR6417885_2.fastq.gz	Fastqsanger.gz
	SRR6417886_1.fastq.gz	Fastqsanger.gz

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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

2018-02-10 | GSE108500 | 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 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.

| S-EPMC6422458 | biostudies-literature

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. 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.

2012-08-01 | E-GEOD-34584 | biostudies-arrayexpress

The role of Foxp1/4 in lung development

2012-08-02 | GSE34584 | GEO

Jarid2 promotes temporal progression of retinal progenitors via repression of Foxp1 [Foxp1 cTG scRNA-seq]

Project description:Transitions in competence underlie the ability of CNS progenitors to generate a diversity of neurons and glia. Retinal progenitor cells in mouse generate early-born cell types embryonically and late-born cell types largely postnatally. We find that the transition from early to late progenitor competence is regulated by Jarid2. Loss of Jarid2 results in extended production of early cell types and extended expression of early progenitor genes. Jarid2 can regulate histone modifications, and we find reduction of repressive mark H3K27me3 on a subset of early progenitor genes with loss of Jarid2, most notably Foxp1. We show that Foxp1 regulates the competence to generate early-born retinal cell types, promotes early and represses late progenitor gene expression, and is required for extending early retinal cell production after loss of Jarid2. We conclude Jarid2 facilitates progression of retinal progenitor temporal identity by repressing Foxp1, which is a primary regulator of early temporal patterning.

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Jarid2 promotes temporal progression of retinal progenitors via repression of Foxp1 [Foxp1 cKO bulk RNA-seq]

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Jarid2 promotes temporal progression of retinal progenitors via repression of Foxp1 [Foxp1 cTG scRNA-seq]

Project description:Jarid2 promotes temporal progression of retinal progenitors via repression of Foxp1 [Foxp1 cTG scRNA-seq]

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

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Gene expression in human umbilical cord endothelial cells following FoxP1 knockdown

Project description:To search for genes regulated by the transcription factor Forkhead box Protein P1 (FoxP1) in endothelial cells, we transfected human umbilical cord endothelial cells (HUVECs) with a combination of three siRNA oligonucleotides directed against human FoxP1 . Human umbilical vein endothelial cells (HUVECs) were isolated from donated umbilical cords, pooled from two donors and cultivated up to passage 5. For transfection with FoxP1-siRNA cells were cultured to 70% confluence and transfected with a combination of three FoxP1-targeting siRNAs or an irrelevant control oligonucleotide (all from invitrogen) using Lipofectamin RNAiMax (Invitrogen) according to the manufacturers instructions. Total RNA was isolated 48h after transfection. Three individual samples per condition were analyzed.

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Glucose deprivation promotes de-differentiation in lung adenocarcinoma

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