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Steroid Hormone Regulatory Mechanism

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Endocrinology and Metabolism".

Deadline for manuscript submissions: closed (31 December 2022) | Viewed by 2005

Special Issue Editors


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Guest Editor
Departments of Biochemistry, School of Medicine, Keio University, Tokyo 160-8582, Japan
Interests: biochemistry; analytical chemistry; mass spectrometry; lipidomics; metabolomics; proteomics
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Guest Editor
Department of Uro-Oncology, Saitama Medical University International Medical Center, Saitama, Japan
Interests: renal cell carcinoma; targeted therapy; aldosterone production

Special Issue Information

Dear Colleagues,

The main mechanism of action of steroid hormones is considered to be the endocrine system, in which steroids are synthesized in endocrine organs under the control of the central nervous system and transported throughout the body to act on target cells. Recently, however, mechanisms of action other than the endocrine secretion of steroid hormones have been reported.

In this Special Issue, we will focus on the mechanisms of action of such steroid hormones. We will also focus on cases where the mode of action and the molecular species involved change depending on the disease. Also included in the scope of this issue are new techniques for visualizing steroid hormones acting on the microenvironment of organs and the structural biology of synthetic enzymes (regioselective control of catalytic activity).

The goal of this issue is to deepen the discussion on new mechanisms of steroid production and their mode of action, as well as on their physiological effects, without being bound by conventional concepts, aiming for the further development of research in this area.

Prof. Dr. Yuki Sugiura
Dr. Koshiro Nishimoto
Guest Editors

Manuscript Submission Information

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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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

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Keywords

  • steroid hormones
  • steroidogenesis
  • steroid production
  • regulation
  • physiological effects
  • mechanisms

Published Papers (1 paper)

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Research

15 pages, 2615 KiB  
Article
HSD3B1 Expression Is Upregulated by Interleukin 4 in HT-29 Colon Cancer Cells via Multiple Signaling Pathways
by Hsin-Mei Chen, Pei-Yu Hung, Chih-Hung Chen, Yu-Jhen Yu, Ming-Shan Syu and Meng-Chun Hu
Int. J. Mol. Sci. 2022, 23(21), 13572; https://doi.org/10.3390/ijms232113572 - 5 Nov 2022
Viewed by 1786
Abstract
3β-Hydroxysteroid dehydrogenase/isomerase is essential for the synthesis of active steroid hormones. Interleukin 4 (IL4) induces the expression of HSD3B1 in various human cancer cell lines. Here, we demonstrated that administration of IL4 to an HT-29 colon cancer cell line induced high expression of [...] Read more.
3β-Hydroxysteroid dehydrogenase/isomerase is essential for the synthesis of active steroid hormones. Interleukin 4 (IL4) induces the expression of HSD3B1 in various human cancer cell lines. Here, we demonstrated that administration of IL4 to an HT-29 colon cancer cell line induced high expression of HSD3B1 at the mRNA and protein levels. In the HT-29 cells, IL4 stimulated the activity of signal transducer and activator of transcription 6 (STAT6) and promoted its binding to the STAT6-binding site in the HSD3B1 promoter. The STAT6 inhibitor significantly suppressed HSD3B1 induction by IL4 in a dose-dependent manner. Moreover, inhibition of the PI3-kinase/AKT pathway strongly suppressed the IL4-induced HSD3B1 expression. Glycogen synthase kinase 3 (GSK3), a downstream target of AKT, had a stimulatory effect on the IL4-induced HSD3B1 expression. However, IL4 stimulated the phosphorylation of AKT, which inhibited the GSK3 activity at the early stage. Hence, GSK3 potentiated the HSD3B1 levels at the late stage of the IL4 stimulation. Additionally, inhibitors of mitogen-activated protein kinases (MAPKs), ERK1/2 and p38, but not of JNK, partly reduced the HSD3B1 expression following the IL4 stimulation. We further demonstrated that IL4 potently promoted steroid synthesis. Our results indicate that IL4 induces HSD3B1 expression via multiple signaling pathways in HT-29 cells and may play a role in the regulation of steroid synthesis. Full article
(This article belongs to the Special Issue Steroid Hormone Regulatory Mechanism)
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