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FOXA2 suppresses endometrial carcinogenesis and epithelial-mesenchymal transition by regulating enhancer activity

ABSTRACT: FOXA2 suppresses endometrial carcinogenesis and epithelial-mesenchymal transition by regulating enhancer activity

PROVIDER: PRJNA795166 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17468120.fastq.gz	Fastqsanger.gz
	SRR17468121.fastq.gz	Fastqsanger.gz
	SRR17468122.fastq.gz	Fastqsanger.gz
	SRR17468123.fastq.gz	Fastqsanger.gz

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FOXA2 suppresses endometrial carcinogenesis and epithelial-mesenchymal transition by regulating enhancer activity

Project description:FOXA2 encodes a transcription factor mutated in 10% of endometrial cancers (ECs), with a higher mutation rate in aggressive variants. FOXA2 has essential roles in embryonic and uterine development. However, FOXA2’s role in EC is incompletely understood. Functional investigations using human and mouse EC cell lines revealed that FOXA2 controls endometrial epithelial gene expression programs regulating cell proliferation, adhesion, and endometrial-epithelial transition. In live animals, conditional inactivation of Foxa2 or Pten alone in endometrial epithelium did not result in ECs, but simultaneous inactivation of both genes resulted in lethal ECs with complete penetrance, establishing potent synergism between Foxa2 and PI3K signaling. Studies in tumor-derived cell lines and organoids highlighted additional invasion and cell growth phenotypes associated with malignant transformation and identified key mediators, including Myc and Cdh1. Transcriptome and cistrome analyses revealed that FOXA2 broadly controls gene expression programs through modification of enhancer activity in addition to regulating specific target genes, rationalizing its tumor suppressor functions. By integrating results from our cell lines, organoids, animal models, and patient data, our findings demonstrated that FOXA2 is an endometrial tumor suppressor associated with aggressive disease and with shared commonalities among its roles in endometrial function and carcinogenesis.

2022-06-14 | GSE193165 | GEO

FOXA2 suppresses endometrial carcinogenesis and epithelial-mesenchymal transition through its actions as chromatin remodeler [WT67]

Project description:FOXA2 encodes a transcription factor mutated in 10% of endometrial cancers (ECs), with a higher mutation rate in aggressive variants. FOXA2 has essential roles in embryonic and uterine development. However, FOXA2’s role in EC is not understood. Functional investigations using human and mouse EC cell lines revealed that FOXA2 controls endometrial epithelial gene expression programs regulating cell proliferation, adhesion, and endometrial-epithelial transition. In live animals, conditional inactivation of Foxa2 or Pten alone in endometrial epithelium did not result in ECs, but simultaneous inactivation of both genes resulted in lethal ECs with complete penetrance, establishing potent synergism between Foxa2 and PI3K signalling. Organoids and tumor-derived cell line studies highlighted additional invasion and cell growth phenotypes associated with malignant transformation and identified key mediators including Myc and Cdh1. Transcriptome and cistrome analyses revealed that FOXA2 broadly controls gene expression programs through chromatin remodeling and modification of enhancer activity in addition to regulating specific target genes, rationalizing its tumor suppressor functions. By integrating results from our cell lines, organoids, animal models, and patient data, our findings demonstrate that FOXA2 is an endometrial tumor suppressor associated with aggressive disease and with shared commonalities among its roles in endometrial function and carcinogenesis.

2022-06-22 | GSE197210 | GEO

FOXA2 suppresses endometrial carcinogenesis and epithelial-mesenchymal transition through its actions as chromatin remodeler [WT41]

Project description:FOXA2 encodes a transcription factor mutated in 10% of endometrial cancers (ECs), with a higher mutation rate in aggressive variants. FOXA2 has essential roles in embryonic and uterine development. However, FOXA2’s role in EC is not understood. Functional investigations using human and mouse EC cell lines revealed that FOXA2 controls endometrial epithelial gene expression programs regulating cell proliferation, adhesion, and endometrial-epithelial transition. In live animals, conditional inactivation of Foxa2 or Pten alone in endometrial epithelium did not result in ECs, but simultaneous inactivation of both genes resulted in lethal ECs with complete penetrance, establishing potent synergism between Foxa2 and PI3K signalling. Organoids and tumor-derived cell line studies highlighted additional invasion and cell growth phenotypes associated with malignant transformation and identified key mediators including Myc and Cdh1. Transcriptome and cistrome analyses revealed that FOXA2 broadly controls gene expression programs through chromatin remodeling and modification of enhancer activity in addition to regulating specific target genes, rationalizing its tumor suppressor functions. By integrating results from our cell lines, organoids, animal models, and patient data, our findings demonstrate that FOXA2 is an endometrial tumor suppressor associated with aggressive disease and with shared commonalities among its roles in endometrial function and carcinogenesis.

2022-06-22 | GSE197209 | GEO

FOXA2 suppresses endometrial carcinogenesis and epithelial-mesenchymal transition through its actions as chromatin remodeler [WT106]

Project description:FOXA2 encodes a transcription factor mutated in 10% of endometrial cancers (ECs), with a higher mutation rate in aggressive variants. FOXA2 has essential roles in embryonic and uterine development. However, FOXA2’s role in EC is not understood. Functional investigations using human and mouse EC cell lines revealed that FOXA2 controls endometrial epithelial gene expression programs regulating cell proliferation, adhesion, and endometrial-epithelial transition. In live animals, conditional inactivation of Foxa2 or Pten alone in endometrial epithelium did not result in ECs, but simultaneous inactivation of both genes resulted in lethal ECs with complete penetrance, establishing potent synergism between Foxa2 and PI3K signalling. Organoids and tumor-derived cell line studies highlighted additional invasion and cell growth phenotypes associated with malignant transformation and identified key mediators including Myc and Cdh1. Transcriptome and cistrome analyses revealed that FOXA2 broadly controls gene expression programs through chromatin remodeling and modification of enhancer activity in addition to regulating specific target genes, rationalizing its tumor suppressor functions. By integrating results from our cell lines, organoids, animal models, and patient data, our findings demonstrate that FOXA2 is an endometrial tumor suppressor associated with aggressive disease and with shared commonalities among its roles in endometrial function and carcinogenesis.

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FOXA2 suppresses endometrial carcinogenesis and epithelial-mesenchymal transition through its actions as chromatin remodeler.

Project description:FOXA2 suppresses endometrial carcinogenesis and epithelial-mesenchymal transition through its actions as chromatin remodeler.

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FOXA2 suppresses endometrial carcinogenesis and epithelial-mesenchymal transition through its actions as chromatin remodeler [WT106]

Project description:FOXA2 suppresses endometrial carcinogenesis and epithelial-mesenchymal transition through its actions as chromatin remodeler [WT106]

| PRJNA809377 | ENA

FOXA2 suppresses endometrial carcinogenesis and epithelial-mesenchymal transition through its actions as chromatin remodeler [WT41]

Project description:FOXA2 suppresses endometrial carcinogenesis and epithelial-mesenchymal transition through its actions as chromatin remodeler [WT41]

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FOXA2 suppresses endometrial carcinogenesis and epithelial-mesenchymal transition through its actions as chromatin remodeler [WT67]

Project description:FOXA2 suppresses endometrial carcinogenesis and epithelial-mesenchymal transition through its actions as chromatin remodeler [WT67]

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ROLE OF HMGA2 IN THE EPITHELIAL TO MESENCHYMAL TRANSITION ASSOCIATED WITH ENDOMETRIAL CARCINOGENESIS

Project description:The molecular events that mediate the epithelial to mesenchymal transition (EMT) in endometrial cancer remain poorly understood. Using cDNA microarrays, we analyzed a group of endometrial carcinosarcomas (ECS), a true example of EMT in vivo, and we compared their gene expression profiles with those obtained from a group of endometrioid endometrial carcinomas (EEC). The HMGA2 gene (High Mobility Group AT-hook 2), an embryonic nuclear factor that mediates EMT in various tumour models, was among the genes overexpressed in ECS, and HMGA2 overexpression was confirmed in 54% of ECSs by qRT-PCR and immunohistochemistry. Moreover, we found a significant inverse correlation between the expression of HMGA2 and let-7b, a member of the let-7 family of miRNAs that represses HMGA2 expression. These changes were also associated with overexpression of Lin28B, a suppressor of microRNA biogenesis implicated in cancer progression and metastasis. Finally, HMGA2 overexpression, which was detected in less than 3% of EECs, was observed in many non-endometrioid carcinomas (46%). For the first time, we describe a role for HMGA2 in both the process of EMT that contributes to endometrial carcinogenesis and in the acquisition of aggressive phenotypes by this neoplasia. Moreover, we demonstrate changes in the expression of genes modulating processes such as EMT, muscle differentiation, the expression of cancer testis antigens (CTAs) and the immune response. Identification of new molecular markers in endometrial carcinogenesis 15 endometrial carcinosarcomas and 23 endometrioid endometrial carcinoma

2012-11-01 | E-GEOD-33723 | biostudies-arrayexpress

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