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Sex Hormone Receptor Signals in Human Malignancies 2.0

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (28 February 2022) | Viewed by 2913

Special Issue Editor


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Guest Editor
Director of Genitourinary Pathology, University of Rochester Medical Center, Rochester, NY, USA
Interests: nuclear hormone receptors; androgen receptor; glucocorticoid receptor; antiandrogens; glucocorticoids; urothelial cancer; prostate cancer; genitourinary pathology
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Special Issue Information

Dear Colleagues,

This Special Issue is the second volume of our previous Special Issue “Sex Hormone Receptor Signals in Human Malignancies”. Sex steroids, including androgens, estrogens, and progestogens, are known to have widespread physiological actions beyond the reproductive system via binding to the sex hormone receptors, members of the nuclear receptor superfamily that function as ligand-inducible transcription factors. Meanwhile, the roles of androgen receptor and estrogen/progesterone receptors have been widely studied in prostate and breast cancers, respectively. However, emerging evidence implies that sex hormone receptor signals play a role in the development and progression of various other types of malignancies, although their exact functions are not fully characterized. These malignancies include, but are not limited to, endometrial cancer, ovarian cancer, urothelial tumor of the bladder or upper urinary tract, liver cancer, lung cancer, and gastrointestinal cancer. Thus, the aim of this Special Issue is to provide an overview of current preclinical and clinical findings indicating the involvement of sex hormone receptor signals in human malignancies that have not traditionally been considered as endocrine neoplasms. Original research or review articles on androgen/estrogen/progesterone receptor signaling in prostate or breast cancer would also be most welcome.

Prof. Dr. Hiroshi Miyamoto
Guest Editor

Manuscript Submission Information

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Keywords

  • androgen receptor
  • estrogen receptor
  • progesterone receptor
  • prostate cancer
  • breast cancer
  • female reproductive system cancer
  • urothelial cancer
  • liver cancer
  • lung cancer
  • gastrointestinal cancer

Published Papers (1 paper)

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Research

13 pages, 2623 KiB  
Article
Androgen Receptor Signaling Induces Cisplatin Resistance via Down-Regulating GULP1 Expression in Bladder Cancer
by Yuki Teramoto, Guiyang Jiang, Takuro Goto, Taichi Mizushima, Yujiro Nagata, George J. Netto and Hiroshi Miyamoto
Int. J. Mol. Sci. 2021, 22(18), 10030; https://doi.org/10.3390/ijms221810030 - 17 Sep 2021
Cited by 13 | Viewed by 2162
Abstract
The underlying molecular mechanisms of resistance to cisplatin-based systemic chemotherapy in bladder cancer patients remain to be elucidated, while the link between androgen receptor (AR) activity and chemosensitivity in urothelial cancer has been implicated. Our DNA microarray analysis in control vs. AR knockdown [...] Read more.
The underlying molecular mechanisms of resistance to cisplatin-based systemic chemotherapy in bladder cancer patients remain to be elucidated, while the link between androgen receptor (AR) activity and chemosensitivity in urothelial cancer has been implicated. Our DNA microarray analysis in control vs. AR knockdown bladder cancer lines identified GULP1 as a potential target of AR signaling. We herein determined the relationship between AR activity and GULP1 expression in bladder cancer cells and then assessed the functional role of GULP1 in cisplatin sensitivity. Androgen treatment in AR-positive cells or AR overexpression in AR-negative cells considerably reduced the levels of GULP1 expression. Chromatin immunoprecipitation further showed direct interaction of AR with the promoter region of GULP1. Meanwhile, GULP1 knockdown sublines were significantly more resistant to cisplatin treatment compared with respective controls. GULP1 knockdown also resulted in a significant decrease in apoptosis, as well as a significant increase in G2/M phases, when treated with cisplatin. In addition, GULP1 was immunoreactive in 74% of muscle-invasive bladder cancers from patients who had subsequently undergone neoadjuvant chemotherapy, including 53% of responders showing moderate (2+)/strong (3+) expression vs. 23% of non-responders showing 2+/3+ expression (P = 0.044). These findings indicate that GULP1 represents a key downstream effector of AR signaling in enhancing sensitivity to cisplatin treatment. Full article
(This article belongs to the Special Issue Sex Hormone Receptor Signals in Human Malignancies 2.0)
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