FOXA1: a transcription factor with parallel functions in development and cancer

Bernardo, Gina M.; Keri, Ruth A.

doi:10.1042/bsr20110046

Cited by 179 publications

(174 citation statements)

References 171 publications

(265 reference statements)

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“…FOXA1 contains conserved nuclear localization sequences and homology in the N-and C-terminal transactivation domains, also. Thus, FOXA1 binding to nucleosomes induces an open chromatin configuration enabling the recruitment of other transcriptional regulators (Bernardo and Keri, 2012). This function has led to FOXA1 being coined as 'pioneering' or 'licensing' factor.…”

Section: Structure and Physiological Function Of Foxa1mentioning

confidence: 99%

FOXA1: a Promising Prognostic Marker in Breast Cancer

Luo²,

Xu³

et al. 2014

Asian Pacific Journal of Cancer Prevention

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Accurate diagnosis and proper monitoring of cancer patients remain important obstacles for successful cancer treatment. The search for cancer biomarkers can aid in more accurate prediction of clinical outcome and may also reveal novel predictive factors and therapeutic targets. One such prognostic marker seems to be FOXA1. Many studies have shown that FOXA1 is strongly expressed in a vast majority of cancers, including breast cancer, in which high expression is associated with a good prognosis. In this review, we summarize the role of this transcription factor in the development and prognosis of breast cancer in the hope of providing insights into utility of FOXA1 as a novel biomarker.

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Section: Structure and Physiological Function Of Foxa1mentioning

confidence: 99%

FOXA1: a Promising Prognostic Marker in Breast Cancer

Luo²,

Xu³

et al. 2014

Asian Pacific Journal of Cancer Prevention

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“…Hnf4α is required for liver (Parviz et al, 2003) and intestinal (Garrison et al, 2006) development, as well as for adult liver function (Hayhurst et al, 2001). Similarly, Foxa1 is involved in both liver and intestinal development and their function (Bernardo and Keri, 2012;van der Sluis et al, 2008). These wide roles across the endoderm lineage are reflected by the broad potential of iHeps, suggesting that an upperlevel endoderm GRN that is normally silent in fibroblasts is engaged by the pioneer factor Foxa1.…”

Section: Understanding Pioneer Factor-driven Direct Lineage Conversiomentioning

confidence: 99%

Direct lineage reprogramming via pioneer factors; a detour through developmental gene regulatory networks

Morris

2016

Development

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Although many approaches have been employed to generate defined fate in vitro, the resultant cells often appear developmentally immature or incompletely specified, limiting their utility. Growing evidence suggests that current methods of direct lineage conversion may rely on the transition through a developmental intermediate. Here, I hypothesize that complete conversion between cell fates is more probable and feasible via reversion to a developmentally immature state. I posit that this is due to the role of pioneer transcription factors in engaging silent, unmarked chromatin and activating hierarchical gene regulatory networks responsible for embryonic patterning. Understanding these developmental contexts will be essential for the precise engineering of cell identity.

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“…FOXA1 contains the forkhead DNA-binding domain and the N-and C-terminal transactivation domains. 7) FOXA1 regulates expression of many genes involved in the development of various tissues, including mammary gland, liver, midbrain, and lung. 8) FOXA1 is also known to function as a chromatin remodeling factor that opens closed chromatin and facilitates the recruitment of other transcription factors.…”

mentioning

confidence: 99%

FOXA1 Induces E-Cadherin Expression at the Protein Level <i>via</i> Suppression of Slug in Epithelial Breast Cancer Cells

Anzai

Hirata

Shibazaki

et al. 2017

Biological & Pharmaceutical Bulletin

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Epithelial-to-mesenchymal transition (EMT) is an important process during embryonic development and tumor progression by which adherent epithelial cells acquire mesenchymal properties. Forkhead box protein A1 (FOXA1) is a transcriptional regulator preferentially expressed in epithelial breast cancer cells, and its expression is lost in mesenchymal breast cancer cells. However, the implication of this biased expression of FOXA1 in breast cancer is not fully understood. In this study, we analyzed the involvement of FOXA1 in EMT progression in breast cancer, and found that stable expression of FOXA1 in the mesenchymal breast cancer MDA-MB-231 cells strongly induced the epithelial marker E-cadherin at the mRNA and protein levels. Furthermore, stable expression of FOXA1 was found to reduce the mRNA and protein expression of Slug, a repressor of E-cadherin expression. FOXA1 knockdown in the epithelial breast cancer MCF7 cells reduced E-cadherin protein expression without decreasing its mRNA expression. In addition, FOXA1 knockdown in MCF7 cells up-regulated Slug mRNA and protein expression. Notably, similar to FOXA1 knockdown, stable expression of Slug in MCF7 cells reduced E-cadherin protein expression without decreasing its mRNA expression. Taken together, these results suggest that although FOXA1 can induce E-cadherin mRNA expression, it preferentially promotes E-cadherin expression at the protein level by suppressing Slug expression in epithelial breast cancer, and that the balance of this FOXA1-Slug axis regulates EMT progression.Key words epithelial-mesenchymal transition; E-cadherin; forkhead box protein A1; Slug; estrogen receptor Epithelial-to-mesenchymal transition (EMT) is a process that converts adherent epithelial cells to motile mesenchymal cells during embryonic development. 1) EMT is also involved in tumor progression through inducing metastasis and chemoresistance in tumor cells.2-4) Therefore, a better understanding of the molecular mechanisms underlying EMT in tumor cells is beneficial for development of novel antitumor agents.E-Cadherin is a crucial protein that mediates cell-cell adhesion in epithelial cells.1) E-Cadherin expression is dramatically reduced during EMT, which causes loss of cell-cell adhesion and gain of cell motility. Reduction in E-cadherin expression is mainly caused by the transcriptional repressors of E-cadherin gene (CDH1).2,5) A major transcriptional repressor of CDH1 is the zinc finger factor Slug. Slug binds to the E-box sequences present in the enhancer region of CDH1 and represses its expression. 6)Forkhead box A1 (FOXA1) is a member of the forkhead box family of transcription factors. FOXA1 contains the forkhead DNA-binding domain and the N-and C-terminal transactivation domains.7) FOXA1 regulates expression of many genes involved in the development of various tissues, including mammary gland, liver, midbrain, and lung. 8) FOXA1 is also known to function as a chromatin remodeling factor that opens closed chromatin and facilitates the recruitment of other transcription fa...

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FOXA1: a transcription factor with parallel functions in development and cancer

Cited by 179 publications

References 171 publications

FOXA1: a Promising Prognostic Marker in Breast Cancer

FOXA1: a Promising Prognostic Marker in Breast Cancer

Direct lineage reprogramming via pioneer factors; a detour through developmental gene regulatory networks

FOXA1 Induces E-Cadherin Expression at the Protein Level <i>via</i> Suppression of Slug in Epithelial Breast Cancer Cells

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