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Cells
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Understanding and Targeting Androgen Receptor Signalling in Prostate Cancer
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Special Issue "Understanding and Targeting Androgen Receptor Signalling in Prostate Cancer"

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cell Signaling".

Deadline for manuscript submissions: closed (31 December 2021) | Viewed by 15479

Special Issue Editor

Dr. Mohammad Asim

E-Mail Website
Guest Editor
Assistant Professor, Department of Clinical & Experimental Medicine, University of Surrey, Surrey, UK
Interests: androgen receptors; prostate cancer; anti-androgens; kinase signalling; synthetic lethality; transcription/translation regulation

Special Issue Information

Dear Colleagues,

This Special Issue is dedicated to consolidating the most up-to-date knowledge of the molecular mechanisms that underlie the development of castration-resistant prostate cancer (CPRC) with a focus on the androgen receptor (AR) signaling axis. It will cover both the cis- and trans- mechanisms of AR activation and their implications in CRPC. This Special Issue not only aims to highlight the signaling upstream of the AR, but also the downstream pathways that manifest prostate cancer progression. By exploiting our understanding of AR-centric disease mechanisms, this Special Issue will present classical therapeutics and upcoming small molecules with the potential to directly as well as though surrogate means target the AR signaling axis. Finally, it will endeavor to provide insight into futuristic therapies to combat newly emerging resistant mechanisms.

Dr. Mohammad Asim
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • molecular mechanisms of androgen receptor activation
  • castration-resistant prostate cancer
  • androgen receptor target pathways relevant to disease progression
  • recent advances in the arsenal of androgen-targeting molecules

Published Papers (5 papers)

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Review

23 pages, 1416 KiB  
Review
Unravelling the Role of Kinases That Underpin Androgen Signalling in Prostate Cancer
by
Katie Joanna Miller
and
Mohammad Asim
Cells 2022, 11(6), 952; https://doi.org/10.3390/cells11060952 - 10 Mar 2022
Cited by 4 | Viewed by 2882
Abstract
The androgen receptor (AR) signalling pathway is the key driver in most prostate cancers (PCa), and is underpinned by several kinases both upstream and downstream of the AR. Many popular therapies for PCa that target the AR directly, however, have been circumvented by [...] Read more.
The androgen receptor (AR) signalling pathway is the key driver in most prostate cancers (PCa), and is underpinned by several kinases both upstream and downstream of the AR. Many popular therapies for PCa that target the AR directly, however, have been circumvented by AR mutation, such as androgen receptor variants. Some upstream kinases promote AR signalling, including those which phosphorylate the AR and others that are AR-regulated, and androgen regulated kinase that can also form feed-forward activation circuits to promotes AR function. All of these kinases represent potentially druggable targets for PCa. There has generally been a divide in reviews reporting on pathways upstream of the AR and those reporting on AR-regulated genes despite the overlap that constitutes the promotion of AR signalling and PCa progression. In this review, we aim to elucidate which kinases—both upstream and AR-regulated—may be therapeutic targets and require future investigation and ongoing trials in developing kinase inhibitors for PCa. Full article
(This article belongs to the Special Issue Understanding and Targeting Androgen Receptor Signalling in Prostate Cancer)
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17 pages, 972 KiB  
Review
Analyzing the Androgen Receptor Interactome in Prostate Cancer: Implications for Therapeutic Intervention
by
Ujjwal R. Dahiya
and
Hannelore V. Heemers
Cells 2022, 11(6), 936; https://doi.org/10.3390/cells11060936 - 09 Mar 2022
Cited by 4 | Viewed by 2319
Abstract
The androgen receptor (AR) is a member of the ligand-activated nuclear receptor family of transcription factors. AR’s transactivation activity is turned on by the binding of androgens, the male sex steroid hormones. AR is critical for the development and maintenance of the male [...] Read more.
The androgen receptor (AR) is a member of the ligand-activated nuclear receptor family of transcription factors. AR’s transactivation activity is turned on by the binding of androgens, the male sex steroid hormones. AR is critical for the development and maintenance of the male phenotype but has been recognized to also play an important role in human diseases. Most notably, AR is a major driver of prostate cancer (CaP) progression, which remains the second leading cause of cancer deaths in American men. Androgen deprivation therapies (ADTs) that interfere with interactions between AR and its activating androgen ligands have been the mainstay for treatment of metastatic CaP. Although ADTs are effective and induce remissions, eventually they fail, while the growth of the majority of ADT-resistant CaPs remains under AR’s control. Alternative approaches to inhibit AR activity and bypass resistance to ADT are being sought, such as preventing the interaction between AR and its cofactors and coregulators that is needed to execute AR-dependent transcription. For such strategies to be efficient, the 3D conformation of AR complexes needs to be well-understood and AR-regulator interaction sites resolved. Here, we review current insights into these 3D structures and the protein interaction sites in AR transcriptional complexes. We focus on methods and technological approaches used to identify AR interactors and discuss challenges and limitations that need to be overcome for efficient therapeutic AR complex disruption. Full article
(This article belongs to the Special Issue Understanding and Targeting Androgen Receptor Signalling in Prostate Cancer)
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19 pages, 1811 KiB  
Review
Androgen Receptor-Mediated Transcription in Prostate Cancer
by
Doğancan Özturan
,
Tunç Morova
and
Nathan A. Lack
Cells 2022, 11(5), 898; https://doi.org/10.3390/cells11050898 - 05 Mar 2022
Cited by 11 | Viewed by 3682
Abstract
Androgen receptor (AR)-mediated transcription is critical in almost all stages of prostate cancer (PCa) growth and differentiation. This process involves a complex interplay of coregulatory proteins, chromatin remodeling complexes, and other transcription factors that work with AR at cis-regulatory enhancer regions to [...] Read more.
Androgen receptor (AR)-mediated transcription is critical in almost all stages of prostate cancer (PCa) growth and differentiation. This process involves a complex interplay of coregulatory proteins, chromatin remodeling complexes, and other transcription factors that work with AR at cis-regulatory enhancer regions to induce the spatiotemporal transcription of target genes. This enhancer-driven mechanism is remarkably dynamic and undergoes significant alterations during PCa progression. In this review, we discuss the AR mechanism of action in PCa with a focus on how cis-regulatory elements modulate gene expression. We explore emerging evidence of genetic variants that can impact AR regulatory regions and alter gene transcription in PCa. Finally, we highlight several outstanding questions and discuss potential mechanisms of this critical transcription factor. Full article
(This article belongs to the Special Issue Understanding and Targeting Androgen Receptor Signalling in Prostate Cancer)
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26 pages, 3920 KiB  
Review
Interaction between Non-Coding RNAs and Androgen Receptor with an Especial Focus on Prostate Cancer
by
Mohammad Taheri
,
Tayyebeh Khoshbakht
,
Elena Jamali
,
Julia Kallenbach
,
Soudeh Ghafouri-Fard
and
Aria Baniahmad
Cells 2021, 10(11), 3198; https://doi.org/10.3390/cells10113198 - 16 Nov 2021
Cited by 8 | Viewed by 2682
Abstract
The androgen receptor (AR) is a member of the nuclear receptor superfamily and has three functional domains, namely the N-terminal, DNA binding, and C-terminal domain. The N-terminal domain harbors potent transactivation functions, whereas the C-terminal domain binds to androgens and antiandrogens used to [...] Read more.
The androgen receptor (AR) is a member of the nuclear receptor superfamily and has three functional domains, namely the N-terminal, DNA binding, and C-terminal domain. The N-terminal domain harbors potent transactivation functions, whereas the C-terminal domain binds to androgens and antiandrogens used to treat prostate cancer. AR has genomic activity being DNA binding-dependent or through interaction with other DNA-bound transcription factors, as well as a number of non-genomic, non-canonical functions, such as the activation of the ERK, AKT, and MAPK pathways. A bulk of evidence indicates that non-coding RNAs have functional interactions with AR. This type of interaction is implicated in the pathogenesis of human malignancies, particularly prostate cancer. In the current review, we summarize the available data on the role of microRNAs, long non-coding RNAs, and circular RNAs on the expression of AR and modulation of AR signaling, as well as the effects of AR on their expression. Recognition of the complicated interaction between non-coding RNAs and AR has practical importance in the design of novel treatment options, as well as modulation of response to conventional therapeutics. Full article
(This article belongs to the Special Issue Understanding and Targeting Androgen Receptor Signalling in Prostate Cancer)
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12 pages, 1366 KiB  
Review
ING Tumour Suppressors and ING Splice Variants as Coregulators of the Androgen Receptor Signalling in Prostate Cancer
by
Anna Melekhova
and
Aria Baniahmad
Cells 2021, 10(10), 2599; https://doi.org/10.3390/cells10102599 - 29 Sep 2021
Cited by 7 | Viewed by 2834
Abstract
Prevention and overcoming castration resistance of prostate cancer (PC) remains one of the main unsolved problems in modern oncology. Hence, many studies are focused on the investigation of novel androgen receptor (AR) regulators that could serve as potential drug targets in disease therapy. [...] Read more.
Prevention and overcoming castration resistance of prostate cancer (PC) remains one of the main unsolved problems in modern oncology. Hence, many studies are focused on the investigation of novel androgen receptor (AR) regulators that could serve as potential drug targets in disease therapy. Among such factors, inhibitor of growth (ING) proteins were identified. Some ING proteins act as AR transcriptional coregulators, indicating their relevance for PC research. The ING family consists of five protein-coding genes from ING1 to ING5 and pseudogene INGX. The ING genes were revealed through their sequence homology to the first identified ING1 from an in vivo screen. ING factors are a part of histone modification complexes. With the help of the conserved plant homeodomain (PHD) motif, ING factors bind to Histone 3 Lysine 4 (H3K4) methylation mark with a stronger affinity to the highest methylation grade H3K4me3 and recruit histone acetyltransferases (HAT) and histone deacetylases (HDAC) to chromatin. ING1 and ING2 are core subunits of mSIN3a-HDAC corepressor complexes, whereas ING3–5 interact with different HAT complexes that serve as coactivators. ING members belong to type II tumour suppressors and are frequently downregulated in many types of malignancies, including PC. As the family name indicates, ING proteins are able to inhibit cell growth and tumour development via regulation of cell cycle and cancer-relevant pathways such as apoptosis, cellular senescence, DNA repair, cell migration, invasion, and angiogenesis. Many ING splice variants that enhance the diversity of ING activity were discovered. However, it seems that the existence of multiple ING splice variants is underestimated, since alternative splice variants, such as the AR coregulators ING1 and ING3, counteract full-length ING and thus play an opposite functional role. These results open a novel prospective investigation direction in understanding ING factors biology in PC and other malignancies. Full article
(This article belongs to the Special Issue Understanding and Targeting Androgen Receptor Signalling in Prostate Cancer)
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