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      FOXA1 and FOXA2: the regulatory mechanisms and therapeutic implications in cancer

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          Abstract

          FOXA1 (Forkhead Box A1) and FOXA2 (Forkhead Box A2) serve as pioneering transcription factors that build gene expression capacity and play a central role in biological processes, including organogenesis and differentiation, glycolipid metabolism, proliferation, migration and invasion, and drug resistance. Notably, FOXA1 and FOXA2 may exert antagonistic, synergistic, or complementary effects in the aforementioned biological processes. This article focuses on the molecular mechanisms and clinical relevance of FOXA1 and FOXA2 in steroid hormone-induced malignancies and highlights potential strategies for targeting FOXA1 and FOXA2 for cancer therapy. Furthermore, the article describes the prospect of targeting upstream regulators of FOXA1/FOXA2 to regulate its expression for cancer therapy because of the drug untargetability of FOXA1/FOXA2.

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          Most cited references188

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          Breast cancer

          Michael Gnant, Nadia Harbeck (2017)
          Breast cancer is one of the three most common cancers worldwide. Early breast cancer is considered potentially curable. Therapy has progressed substantially over the past years with a reduction in therapy intensity, both for locoregional and systemic therapy; avoiding overtreatment but also undertreatment has become a major focus. Therapy concepts follow a curative intent and need to be decided in a multidisciplinary setting, taking molecular subtype and locoregional tumour load into account. Primary conventional surgery is not the optimal choice for all patients any more. In triple-negative and HER2-positive early breast cancer, neoadjuvant therapy has become a commonly used option. Depending on clinical tumour subtype, therapeutic backbones include endocrine therapy, anti-HER2 targeting, and chemotherapy. In metastatic breast cancer, therapy goals are prolongation of survival and maintaining quality of life. Advances in endocrine therapies and combinations, as well as targeting of HER2, and the promise of newer targeted therapies make the prospect of long-term disease control in metastatic breast cancer an increasing reality.
          Article 0 comments Cited 699 times – based on 0 reviews     Review now
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            Chromatin accessibility and the regulatory epigenome

            Sandy L. Klemm, Zohar Shipony, William J Greenleaf (2019)
            Physical access to DNA is a highly dynamic property of chromatin that plays an essential role in establishing and maintaining cellular identity. The organization of accessible chromatin across the genome reflects a network of permissible physical interactions through which enhancers, promoters, insulators and chromatin-binding factors cooperatively regulate gene expression. This landscape of accessibility changes dynamically in response to both external stimuli and developmental cues, and emerging evidence suggests that homeostatic maintenance of accessibility is itself dynamically regulated through a competitive interplay between chromatin-binding factors and nucleosomes. In this Review, we examine how the accessible genome is measured and explore the role of transcription factors in initiating accessibility remodelling; our goal is to illustrate how chromatin accessibility defines regulatory elements within the genome and how these epigenetic features are dynamically established to control gene expression.
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              PROTAC targeted protein degraders: the past is prologue

              Miklos Bekes, David R Langley, Craig M Crews (2022)
              Targeted protein degradation (TPD) is an emerging therapeutic modality with the potential to tackle disease-causing proteins that have historically been highly challenging to target with conventional small molecules. In the 20 years since the concept of a proteolysis-targeting chimera (PROTAC) molecule harnessing the ubiquitin–proteasome system to degrade a target protein was reported, TPD has moved from academia to industry, where numerous companies have disclosed programmes in preclinical and early clinical development. With clinical proof-of-concept for PROTAC molecules against two well-established cancer targets provided in 2020, the field is poised to pursue targets that were previously considered ‘undruggable’. In this Review, we summarize the first two decades of PROTAC discovery and assess the current landscape, with a focus on industry activity. We then discuss key areas for the future of TPD, including establishing the target classes for which TPD is most suitable, expanding the use of ubiquitin ligases to enable precision medicine and extending the modality beyond oncology. Targeted protein degradation with proteolysis-targeting chimeras (PROTACs) has the potential to tackle disease-causing proteins that have historically been highly challenging to target with conventional small molecules. This article summarizes the first two decades of PROTAC discovery and discusses key areas for the future of this therapeutic modality, including establishing the target classes for which it is most suitable and extending its application beyond oncology.
              Article 0 comments Cited 411 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Na Liu:
                ORCID: http://orcid.org/0009-0000-8898-1840
                2697075944@qq.com
                Minbin Chen: cmb1981@163.com
                Journal
                Journal ID (nlm-ta): Cell Death Discov
                Journal ID (iso-abbrev): Cell Death Discov
                Title: Cell Death Discovery
                Publisher: Nature Publishing Group UK (London )
                ISSN (Electronic): 2058-7716
                Publication date (Electronic): 11 April 2024
                Publication date PMC-release: 11 April 2024
                Publication date Collection: 2024
                Volume: 10
                Electronic Location Identifier: 172
                Affiliations
                [1 ]GRID grid.452273.5, ISNI 0000 0004 4914 577X, Department of Radiotherapy and Oncology, , Affiliated Kunshan Hospital of Jiangsu University, ; Kunshan, China
                [2 ]GRID grid.452273.5, ISNI 0000 0004 4914 577X, Department of Radiotherapy and Oncology, Gusu School, Nanjing Medical University, , The First People’s Hospital of Kunshan, ; Suzhou, 215300 Jiangsu Province China
                [3 ]College of Life Sciences, University of Chinese Academy of Sciences, ( https://ror.org/05qbk4x57) Beijing, 100049 China
                Author information
                http://orcid.org/0009-0000-8898-1840
                Article
                Publisher ID: 1936
                DOI: 10.1038/s41420-024-01936-1
                PMC ID: 11009302
                PubMed ID: 38605023
                SO-VID: 5bbd6b8f-44fa-4efb-93ed-a63deff7e48e
                Copyright © © The Author(s) 2024
                License:

                Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

                History
                Date received : 14 January 2024
                Date revision received : 23 March 2024
                Date accepted : 26 March 2024
                Funding
                Funded by: This work was supported by the National Natural Science Foundation (grant no. 82072712); Health Commission Medical Research Program of Jiangsu Province (Z2023096) ; Suzhou Clinical Key Disease Diagnosis and Treatment Technology Program(LCZX202339); Suzhou Science and Technology Development Program(SLT2023020、SKY2023093); Key Healthcare Talent in Gusu District(054).
                Categories
                Subject: Review Article
                Custom metadata
                issue-copyright-statement © Cell Death Differentiation Association (ADMC) 2024

                Keywords: cell death,cancer,cancer genetics
                Data availability:
                Keywords: cell death, cancer, cancer genetics

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