Hormone Receptors in Cancer

A special issue of Biomolecules (ISSN 2218-273X).

Deadline for manuscript submissions: closed (15 March 2019) | Viewed by 6238

Special Issue Editor


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Guest Editor
Tokyo Metropolitan Institute of Gerontology, Department of Functional Biogerontology, Tokyo, Japan
Interests: hormone receptor; nuclear receptor; steroid hormone; epigenetic factor; non-coding RNA; transcription; chromatin; post-transcriptional regulation; non-genomic function; splicing; cell signaling; apoptosis; cell proliferation; invasion; metastasis

Special Issue Information

Dear Colleagues,

Cancer is known to be caused by various environmental factors which transmit intracellular signaling to reduce apoptosis or promote cell cycle for proliferation and invasion. Numerous of studies have reported that hormone receptors play important roles in both the development and progression of cancer. In particular, the dysregulated target signals of estrogen receptor (ER) in breast cancer and androgen receptor (AR) in prostate cancer have been extensively investigated. Although hormone receptors have been shown to be involved in numerous cellular processes, including both at a transcriptional and a non-genomic level, most of them acts as nuclear receptor (NR) to exert its function by binding to specific genomic sites and regulates the target gene expression. Recently, the central role of chromatin structure and epigenetic modification in NR-mediated gene regulation has been highlighted. NR such as ER and AR functions through interaction with tissue-specific transcription factors such as forkhead box protein A1 (FOXA1). Epigenetic changes including altered DNA methylation, histone modification, and chromatin remodeling are induced upon NR recruitment. Interestingly, non-coding RNAs such as long non-coding RNAs (lncRNAs) and micro RNAs (miRNAs) also modulate epigenetic status through NR function directly or indirectly. Mutation or dysregulated expression of these epigenetic modifiers has been observed in clinical studies. Moreover, recent advances in nuclear receptor researches have shown that increased expression of splice variants, and protein level modifications such as ubiquitylation and phosphorylation were found to be key events in NR signaling and cancer progression.

This Special Issue focuses on understanding various molecular mechanisms to regulate hormone receptor functions, such as post-translational modification or epigenetic regulation in cancer genome. Target effects by these transcriptional or non-genomic programs to promote cell proliferation, epithelial-mesenchymal transition, enhance migratory potential and altered metabolism in cancer cells will also be discussed. We welcome experts in the field to contribute research papers and critical reviews on the various facets of hormone receptor signaling in human cancers for increasing our knowledge, as well as on how clinical data may be exploited as tools in developing anti-cancer therapies and new biomarkers. Studies associated with any kind of hormones and any type of cancer will be accepted.

Dr. Kenichi Takayama
Guest Editor

Manuscript Submission Information

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Keywords

  • hormone receptor
  • nuclear receptor
  • steroid hormone
  • epigenetic factor
  • non-coding RNA
  • transcription
  • chromatin
  • post-transcriptional regulation
  • non-genomic function
  • splicing
  • cell signaling
  • apoptosis
  • cell proliferation
  • invasion
  • metastasis

Published Papers (1 paper)

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Review

15 pages, 1442 KiB  
Review
Splicing Factors Have an Essential Role in Prostate Cancer Progression and Androgen Receptor Signaling
by Ken-ichi Takayama
Biomolecules 2019, 9(4), 131; https://doi.org/10.3390/biom9040131 - 1 Apr 2019
Cited by 39 | Viewed by 5870
Abstract
Although inhibition of the androgen–androgen receptor (AR) axis effectively represses the growth of prostate cancer, most of all cases eventually become castration-resistant prostate cancers (CRPCs). Enhancement of the expression of AR and its variants along with the downstream signals is important for disease [...] Read more.
Although inhibition of the androgen–androgen receptor (AR) axis effectively represses the growth of prostate cancer, most of all cases eventually become castration-resistant prostate cancers (CRPCs). Enhancement of the expression of AR and its variants along with the downstream signals is important for disease progression. AR-V7, a constitutive active form of AR, is generated as a result of RNA splicing. RNA splicing creates multiple transcript variants from one pre-messenger RNA (mRNA) by removing introns/exons to allow mRNA translation. The molecular mechanisms leading to marked increases of AR and generation of AR-V7 have been unclear. However, recent papers highlighted the roles of RNA splicing factors which promote AR expression and production of variants. Notably, a broad range of splicing components were aberrantly regulated in CRPC tissues. Interestingly, expression of various spliceosome genes is enhanced by RNA-binding protein splicing factor proline- and glutamine-rich (PSF/SFPQ), leading to changes in the expression of AR transcript variants. Moreover, inhibition of several splicing factors repressed tumor growth in vivo. Altered expression of splicing factors is correlated to biochemical recurrence in prostate cancer patients. Thus, these findings suggest that splicing factors would be a potential therapeutic target. This review focuses on the emerging roles of splicing factors in prostate cancer progression and AR signaling. Full article
(This article belongs to the Special Issue Hormone Receptors in Cancer)
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