Mechanism of Nuclear Hormone Receptors in Cancer II

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

Deadline for manuscript submissions: closed (25 February 2024) | Viewed by 2397

Special Issue Editors


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Guest Editor
Department of Systems Aging Science and Medicine, Tokyo Metropolitan Institute of Gerontology, Itabashi-ku, Tokyo 173-0015, Japan
Interests: hormone-dependent cancers; steroid hormone receptors; estrogen; androgen
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Guest Editor
Department of Geriatric Medicine, Graduate School of Medicine, the University of Tokyo, Bunkyo-ku, Tokyo 113-8655, Japan
Interests: estrogen receptor; breast cancer; osteoporosis; vitamin K
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The relationship between hormones and cancer has a long history that can be traced back to the 19th century when Dr. Beatson treated a breast cancer patient by ovariectomy in 1896. In 1941, Dr. Huggins performed orchidectomy and administered estrogen to a prostate cancer patient, which led to his receipt of the Nobel Prize in 1966. In 1971, tamoxifen came into clinical use as an endocrine therapy for breast cancer. Interestingly, the clinical use of tamoxifen preceded the molecular cloning of the estrogen receptor in 1986. Now, we understand the importance of estrogen receptors and the androgen receptor as transcription factors in the pathogenesis of breast cancer and prostate cancer. Investigations of novel mechanisms of these receptors, such as nongenomic actions or post-transcriptional modifications, are ongoing.

The estrogen receptors and the androgen receptor belong to the nuclear receptor superfamily. Several members of this superfamily are classified as steroid or other hormone receptor subfamilies. In relation with malignancies, their ligands including glucocorticoids and retinoic acid are clinically used for lymphoma and leukemia. In addition, it has been suggested that nuclear receptors without corresponding steroid ligands or orphan nuclear receptors whose endogenous ligands have not been discovered are involved in the mechanism of cancer development.

This Special Issue aims to summarize current knowledge on the nuclear hormone receptors in relation to cancer biology. We invite experts in this field to submit original research papers or reviews on the various nuclear receptors in human cancers. A wide range of studies, from basic to clinical research, are welcome.

Prof. Dr. Satoshi Inoue
Dr. Kotaro Azuma
Guest Editors

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Keywords

  • hormone
  • nuclear receptor
  • genetics
  • transcription
  • RNA regulation
  • epigenetics
  • protein modification
  • cancer
  • metabolomics
  • breast
  • prostate
  • uterus
  • ovary
  • testis
  • endocrine-related cancer
  • hormone therapy
  • refractory cancer
  • CRPC

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Published Papers (1 paper)

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Research

15 pages, 2137 KiB  
Article
Estrogen-Inducible LncRNA BNAT1 Functions as a Modulator for Estrogen Receptor Signaling in Endocrine-Resistant Breast Cancer Cells
by Kuniko Horie, Kiyoshi Takagi, Toshihiko Takeiwa, Yuichi Mitobe, Hidetaka Kawabata, Takashi Suzuki, Kazuhiro Ikeda and Satoshi Inoue
Cells 2022, 11(22), 3610; https://doi.org/10.3390/cells11223610 - 15 Nov 2022
Cited by 10 | Viewed by 1992
Abstract
Recent advances in RNA studies have revealed that functional long noncoding RNAs (lncRNAs) contribute to the biology of cancers. In breast cancer, estrogen receptor α (ERα) is an essential transcription factor that primarily promotes the growth of luminal-type cancer, although only a small [...] Read more.
Recent advances in RNA studies have revealed that functional long noncoding RNAs (lncRNAs) contribute to the biology of cancers. In breast cancer, estrogen receptor α (ERα) is an essential transcription factor that primarily promotes the growth of luminal-type cancer, although only a small number of lncRNAs are identified as direct ERα targets and modulators for ERα signaling. In this study, we performed RNA-sequencing for ER-positive breast cancer cells and identified a novel estrogen-inducible antisense RNA in the COL18A1 promoter region, named breast cancer natural antisense transcript 1 (BNAT1). In clinicopathological study, BNAT1 may have clinical relevance as a potential diagnostic factor for prognoses of ER-positive breast cancer patients based on an in situ hybridization study for breast cancer specimens. siRNA-mediated BNAT1 silencing significantly inhibited the in vitro and in vivo growth of tamoxifen-resistant ER-positive breast cancer cells. Notably, BNAT1 silencing repressed cell cycle progression whereas it promoted apoptosis. Microarray analysis revealed that BNAT1 silencing in estrogen-sensitive breast cancer cells repressed estrogen signaling. We showed that BNAT1 knockdown decreased ERα expression and repressed ERα transactivation. RNA immunoprecipitation showed that BNAT1 physically binds to ERα protein. In summary, BNAT1 would play a critical role in the biology of ER-positive breast cancer by modulating ERα-dependent transcription regulation. We consider that BNAT1 could be a potential molecular target for diagnostic and therapeutic options targeting luminal-type and endocrine-resistant breast cancer. Full article
(This article belongs to the Special Issue Mechanism of Nuclear Hormone Receptors in Cancer II)
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