Cited by 22Estrogen and related hormone effectsSkin Protection and AgingNonmelanoma Skin Cancer Studies

Oestrogen receptor-β signalling protects against transplanted skin tumour growth in the mouse

Cho, Jun-Lae, Allanson, Munif, Reeve, Vivienne E.·2010·Photochemical & Photobiological Sciences

Abstract

We have reported previously that a deficiency in signalling by the non-classical oestrogen receptor-beta (Er-beta) exacerbates immunosuppression by UV radiation in the mouse. Because photoimmune suppression is a risk factor for skin cancer development, we hypothesize that Er-beta deficiency will promote skin tumour growth. Therefore we have blocked Er signalling pharmacologically in the Skh:hr-1 hairless mouse by topical treatments with the Er antagonist ICI 182,780, and genetically in haired mice by using the specific Er-beta knockout mouse (targeted mutation of the Er-beta), and examined the growth rate of 3 transplantable skin tumour cell lines in their syngeneic host mice. Two UV-induced squamous cell carcinoma (SCC) cell lines transplanted into the Skh:hr-1 recipients were found to have regressor qualities that were delayed by prior immunosuppressive solar-simulated UV (SSUV) irradiation. For the T79 SCC, regression was significantly further delayed by combined pretreatment with SSUV+ICI 182,780, and the diameters of the surviving tumours were slightly larger. For the KL3.0 SCC, both SSUV and combined SSUV+ICI 182,780 pretreatments completely inhibited tumour regression, and resulted in significantly greater tumour diameters than in unirradiated recipient mice. In heterozygous Er-beta deficient mice (Er-beta+/-), the B16/F10 melanoma grew progressively and significantly faster than in the wild type control mice (C57BL/6), and growth rate was accelerated by prior SSUV irradiation. Homozygous Er-beta-/- mice supported the most rapid B16/F10 growth that was further accelerated by prior SSUV irradiation. Therefore Er signalling, specifically by Er-beta, has a natural endogenous protective role against skin tumour growth, probably mediated via immunological pathways.

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Crossref · 10.1039/b9pp00168a

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Authors
Cho, J.-L., Allanson, M., & Reeve, V. E.
Affiliations
The University of Sydney (AU)
Corresponding author
Reeve, Vivienne E.
Venue
Photochemical & Photobiological Sciences
Published
2010-04
Volume
9
Issue
4
Pages
608-614
ISSN
  • 1474-905X (ISSN-L)
  • 1474-9092
OpenAlex
W2031621131
Cited by
22
References
28
Citations by year
2024: 1 · 2023: 1 · 2021: 2 · 2020: 2 · 2018: 2 · 2017: 1 · 2016: 2 · 2015: 3 · 2014: 3 · 2012: 2
FWCI
0.90
Type
journal article
Language
en
Open access
closed
Locations
  • Photochemical & Photobiological Sciences (publishedVersion)
  • PubMed (publishedVersion)
Funders
Cancer Council NSW
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Estrogen and related hormone effects
  • Health Sciences › Medicine › Dermatology › Skin Protection and Aging
  • Health Sciences › Medicine › Epidemiology › Nonmelanoma Skin Cancer Studies
Keywords
estrogen receptor beta, estrogen signaling, squamous cell carcinoma, melanoma, UV-induced immunosuppression, fulvestrant, tumor regression
MeSH terms
Fulvestrant, Animals, Cell Transformation, Neoplastic, Dermatitis, Contact, Estradiol, Female, Humans, Neoplasm Transplantation, Skin Neoplasms, Ultraviolet Rays, Cell Line, Tumor, Estrogen Receptor beta, Cell Proliferation, Mice, Gene Knockout Techniques

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