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

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus Homo sapiens

PROVIDER: GSE197211 | GEO | 2022/06/22

REPOSITORIES: GEO

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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]

2022-06-22 | GSE197209 | GEO

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

2022-06-22 | GSE197208 | GEO

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.

| PRJNA809368 | ENA

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]

| PRJNA809376 | ENA

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]

| PRJNA809375 | ENA

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 by regulating enhancer activity

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

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DACH1 suppresses epithelial to mesenchymal transition (EMT) through Notch1 pathway and reverses progestin resistance in endometrial carcinoma.

Project description:Progestin resistance limits the effectiveness of progestin therapy in endometrial carcinoma for patients who desire to preserve fertility. To investigate the molecular mechanism of progestin resistance in endometrial carcinoma, we performed microarray analysis among Ishikawa and progestin resistant cell IshikawaPR cells. We found that epithelial to mesenchymal transition (EMT) was involved in progestin resistance and dachshund family transcription factor 1 (DACH1) is positively correlated with progesterone receptor (PGR). Knockdown of DACH1 in Ishikawa cell promoted proliferation, metastasis ability, and resistance to progestin. Conversely, overexpression of DACH1 in IshikawaPR cell rendered more sensitive to progestin treatment. Xenograft model assay also had similar results. In addition, our data showed that DACH1 overexpression inhibited EMT and decreased c-Jun, Notch1 and Hes1expression. Our study demonstrated for the first time that EMT is involved in progestin resistance of EC. The response to progestin could be reserved by DACH1 suppressed EMT through Notch1 pathway via c-Jun.

| S-EPMC6675747 | biostudies-literature

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