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FOXA1 is a master factor in controlling the TGF-beta-stimulated transcriptome and a regulator of TGF-beta biological functions in nasopharyngeal carcinoma oncogenesis.
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FOXA1 mutations alter its pioneering function and perturb normal luminal epithelial differentiation programs, providing further support for the role of lineage plasticity in prostate cancer progression
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description of central role of FOXA1 in mediating oncogenesis driven by the androgen receptor, and mechanistic insights into how the classes of FOXA1 alteration promote the initiation and/or metastatic progression of prostate cancer; results have direct implications for understanding the pathobiology of other hormone-receptor-driven cancers and rationalize the co-targeting of FOXA1 activity in therapeutic strategies
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Study find that FOXA1 is an important mediator of proliferative and antiapoptotic activities in human colorectal cancer cells. FOXA1 was upregulated in human colorectal cancer tissues and was associated with poor prognosis, suggesting an oncogenic role of FOXA1 in the development and progression of human colorectal cancer.
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FOXA1 is expressed in more than 50% of ER+ breast cancers. Similar studies show that FOXA1 is required for estrogen-induced re-entry into the cell cycle
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AR + /FOXA1 + expression defines a luminal-like TNBC subgroup affected with a worse outcome compared to other TNBC and a higher risk of late recurrences. This subgroup appears enriched in PIK3CA mutations, suggesting a role for PI3K inhibitors in this subgroup.
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FOXA1 promoted proliferation, migration, invasion, and decreased chemosensitivity of gastric cancer cells to 5-Fu treatment through transcriptional activator KRT7
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a compact palindromic DNA element (termed 'DIV' for its diverging half-sites) induces the homodimerization of FOXA1 with strongly positive cooperativity. Collectively, the DIV guides chromatin engagement and regulation by FOXA1 and its perturbation could be linked to disease etiologies.
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the functional genetic variant rs4442975 (FOXA1)was associated with bone marrow suppression during neoadjuvant chemotherapy for luminal A type breast cancer. These results may help establish reliable molecular markers for predicting the prognosis of personalized treatment for luminal A type breast cancer and thereby contribute to the development of appropriate therapies.
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CK7 expression is an independent prognostic factor for esophageal squamous cell carcinoma, and FOXA1 is a non-independent prognostic factor.
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FOXA1 was expressed mostly in ER-positive breast cancer metastases. Expression of Nestin was related to triple-negative metastases, where brain was the most frequent metastatic site. These findings highlight the clinical utility of FOXA1 and Nestin expression and warrant their inclusion in routine immunohistochemical panels for breast carcinoma.
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Circular RNA MCM3AP-AS1 directly bound to miR-194-5p and acted as competing endogenous RNA while subsequently facilitating miR-194-5p target gene FOXA1 expression in hepatocellular carcinoma cells.
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Here we identify the transcription factor ONECUT2 (OC2) as a master regulator of AR networks in metastatic castration-resistant prostate cancer (mCRPC). OC2 acts as a survival factor in mCRPC models, suppresses the AR transcriptional program by direct regulation of AR target genes and the AR licensing factor FOXA1, and activates genes associated with neural differentiation and progression to lethal disease.
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the expression level of miR-132 was decreased in thyroid cancer tissues and cell lines and that miR-132 inhibited cell proliferation, migration, and invasion of thyroid cancer by repressing FOXA1.
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these results provide a mechanism for how interdependent FoxO1:FoxA1/2 binding is negatively impacted by insulin and provide a developmental context for cooperative gene activation by these factors.
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Mammary Paget's disease and extramammary (EMPD) share dysregulation of the glandular developmental regulator gene FOXA1
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FoxA1 and FoxA2 drive gastric differentiation and suppress squamous identity in NKX2-1-negative lung cancer.
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We show that MSK1 downregulation impairs the differentiation of breast cancer cells, increasing their bone homing and growth capacities. MSK1 controls the expression of genes required for luminal cell differentiation, including the GATA3 and FOXA1 transcription factors, by modulating their promoter chromatin status.
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The cell cycle control kinase CDK1 might control directly FOXA1 by phosphorylation and other kinases indirectly by means of regulating other proteins.
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The unexpected signature for estradiol-induced program resides in indirect recruitment of ERa to a large cohort of basally active FOXA1-bound enhancers that lack cognate ERa DNA-binding elements.