Blocking 17β-hydroxysteroid dehydrogenase type 1 in endometrial cancer: A potential novel endocrine therapeutic approach
Open accessAbstract
The enzyme type 1 17β-hydroxysteroid dehydrogenase (17β-HSD-1), responsible for generating active 17β-estradiol (E2) from low-active estrone (E1), is overexpressed in endometrial cancer (EC), thus implicating an increased intra-tissue generation of E2 in this estrogen-dependent condition. In this study, we explored the possibility of inhibiting 17β-HSD-1 and impairing the generation of E2 from E1 in EC using in vitro, in vivo, and ex vivo models. We generated EC cell lines derived from the well-differentiated endometrial adenocarcinoma Ishikawa cell line and expressing levels of 17β-HSD-1 similar to human tissues. In these cells, HPLC analysis showed that 17β-HSD-1 activity could be blocked by a specific 17β-HSD-1 inhibitor. In vitro, E1 administration elicited colony formation similar to E2, and this was impaired by 17β-HSD-1 inhibition. In vivo, tumors grafted on the chicken chorioallantoic membrane (CAM) demonstrated that E1 upregulated the expression of the estrogen responsive cyclin A similar to E2, which was impaired by 17β-HSD-1 inhibition. Neither in vitro nor in vivo effects of E1 were observed using 17β-HSD-1-negative cells (negative control). Using a patient cohort of 52 primary ECs, we demonstrated the presence of 17β-HSD-1 enzyme activity (ex vivo in tumor tissues, as measured by HPLC), which was inhibited by over 90% in more than 45% of ECs using the 17β-HSD-1 inhibitor. Since drug treatment is generally indicated for metastatic/recurrent and not primary tumor, we next demonstrated the mRNA expression of the potential drug target, 17β-HSD-1, in metastatic lesions using a second cohort of 37 EC patients. In conclusion, 17β-HSD-1 inhibition efficiently blocks the generation of E2 from E1 using various EC models. Further preclinical investigations and 17β-HSD-1 inhibitor development to make candidate compounds suitable for the first human studies are awaited. Copyright © 2017 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
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The FP4643 type 1 inhibitor inhibits 17βHSD1 enzyme activity in in vitro and ex vivo models.
“had promising results demonstrating the inhibition of enzyme activity using the FP4643 type 1 inhibitor in both in vitro and ex vivo models.”
From Endometrial Intracrinology: Oestrogens, Androgens and Endometrial Disorders (2018) · cites this paper as [104]
17βHSD1 is detected in endometrial cancer metastatic lesions.
“Konings et al. [104] reported detection of 17βHSD1 in EC metastatic lesions”
From Endometrial Intracrinology: Oestrogens, Androgens and Endometrial Disorders (2018) · cites this paper as [104]
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- Authors
- Konings, G. F., Cornel, K. M., Xanthoulea, S., Delvoux, B., Skowron, M. A., Kooreman, L., Koskimies, P., Krakstad, C., Salvesen, H. B., van Kuijk, K., Schrooders, Y. J., Vooijs, M., Groot, A. J., Bongers, M. Y., Kruitwagen, R. F., ENITEC, & Romano, A.
- Affiliations
- Maastricht University Medical Centre (NL)
- Heinrich Heine University Düsseldorf (DE)
- Forendo Pharma Ltd Turku Finland
- Haukeland University Hospital (NO)
- GROW – School for Oncology and Developmental Biology Maastricht University The Netherlands
- Maastricht University (NL)
- Corresponding author
- Romano, Andrea
- ORCID
- Venue
- The Journal of Pathology
- Publisher
- Wiley
- Published
- 2018-01-03
- Volume
- 244
- Issue
- 2
- Pages
- 203-214
- ISSN
- 0022-3417 (ISSN-L)
- 1096-9896
- OpenAlex
- W2769122162
- Cited by
- 26
- References
- 48
- Citations by year
- 2026: 2 · 2025: 2 · 2024: 2 · 2023: 3 · 2022: 3 · 2021: 4 · 2020: 1 · 2018: 9
- FWCI
- 1.82
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- The Journal of Pathology (publishedVersion)
- PubMed (publishedVersion)
- Research Publications (Maastricht University) (acceptedVersion, other-oa)
- Research Publications (Maastricht University) (submittedVersion, other-oa)
- Funders
- KWF Kankerbestrijding (UM-13-5782)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Estrogen and related hormone effects
- Health Sciences › Medicine › Obstetrics and Gynecology › Endometrial and Cervical Cancer Treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Lipids, and Metabolism
- Keywords
- endometrial cancer, estrone, estradiol, enzyme inhibition, endocrine therapy, estrogen metabolism, Ishikawa cells, chicken chorioallantoic membrane, cyclin A, metastasis
- MeSH terms
- Aged, Aged, 80 and over, Animals, Antineoplastic Agents, Chick Embryo, Enzyme Inhibitors, Estradiol, Estradiol Dehydrogenases, Estrone, Female, Humans, Middle Aged, Signal Transduction, Endometrial Neoplasms, Cyclin A, Cell Line, Tumor, Cell Proliferation, Molecular Targeted Therapy
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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