The inhibition of steroid hormones determines the fate of IPC-366 tumor cells, highlighting the crucial role of androgen production in tumor processes

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dc.contributor.authorCrespo, Belen
dc.contributor.authorCáceres Ramos, Sara Cristina
dc.contributor.authorSilván Granado, Gema
dc.contributor.authorIllera Del Portal, Josefina María
dc.contributor.authorIllera Del Portal, Juan Carlos
dc.date.accessioned2024-01-31T08:25:55Z
dc.date.available2024-01-31T08:25:55Z
dc.date.issued2023-06-01
dc.descriptionCRediT authorship contribution statement Belen Crespo: Conceptualization, Methodology, Writing – original draft, Writing – review & editing. Sara Caceres: Conceptualization, Methodology, Writing – original draft, Writing – review & editing. Gema Silvan: Methodology, Writing – review & editing. Maria Jose Illera: Methodology, Writing – review & editing. J.C. Illera: Conceptualization, Methodology, Writing – original draft, Writing – review & editing.
dc.description.abstractInflammatory mammary cancer (IMC) is a disease that affects female dogs. It is characterized by poor treatment options and no efficient targets. However, anti-androgenic and anti-estrogenic therapies could be effective because IMC has a great endocrine influence, affecting tumor progression. IPC-366 is a triple negative IMC cell line that has been postulated as a useful model to study this disease. Therefore, the aim of this study was to inhibit steroid hormones production at different points of the steroid pathway in order to determine its effect in cell viability and migration in vitro and tumor growth in vivo. For this purpose, Dutasteride (anti-5αReductase), Anastrozole (anti-aromatase) and ASP9521 (anti-17βHSD) and their combinations have been used. Results revealed that this cell line is positive to estrogen receptor β (ERβ) and androgen receptor (AR) and endocrine therapies reduce cell viability. Our results enforced the hypothesis that estrogens promote cell viability and migration in vitro due to the function of E1SO4 as an estrogen reservoir for E2 production that promotes the IMC cells proliferation. Also, an increase in androgen secretion was associated with a reduction in cell viability. Finally, in vivo assays showed large tumor reduction. Hormone assays determined that high estrogen levels and the reduction of androgen levels promote tumor growth in Balb/SCID IMC mice. In conclusion, estrogen levels reduction may be associated with a good prognosis. Also, activation of AR by increasing androgen production could result in effective therapy for IMC because their anti-proliferative effect.
dc.description.departmentDepto. de Fisiología
dc.description.facultyFac. de Veterinaria
dc.description.refereedTRUE
dc.description.sponsorshipMinisterio de Ciencia, Inovacion y Universidades
dc.description.sponsorshipInstituto de Salud Carlos III
dc.description.statuspub
dc.identifier.citationCrespo, B., Caceres, S., Silvan, G., Illera, M. J., & Illera, J. C. (2023). The inhibition of steroid hormones determines the fate of IPC-366 tumor cells, highlighting the crucial role of androgen production in tumor processes. Research in veterinary science, 161, 1–14. https://doi.org/10.1016/j.rvsc.2023.05.014
dc.identifier.doi10.1016/j.rvsc.2023.05.014
dc.identifier.issn0034-5288
dc.identifier.officialurlhttps://www.sciencedirect.com/science/article/pii/S003452882300156X?via%3Dihub
dc.identifier.pmid37290206
dc.identifier.urihttps://hdl.handle.net/20.500.14352/96857
dc.journal.titleResearch in Veterinary Sciences
dc.language.isoeng
dc.page.final14
dc.page.initial1
dc.publisherElsevier
dc.relation.projectIDPI22/ 00314
dc.rightsAttribution 4.0 Internationalen
dc.rights.accessRightsopen access
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.subject.cdu576
dc.subject.keywordAndrogen
dc.subject.keywordEstrogen
dc.subject.keywordSteroid pathway
dc.subject.keywordInflammatory mammary cancer
dc.subject.ucmBiología celular (Biología)
dc.subject.unesco2407.01 Cultivo Celular
dc.titleThe inhibition of steroid hormones determines the fate of IPC-366 tumor cells, highlighting the crucial role of androgen production in tumor processes
dc.typejournal article
dc.type.hasVersionVoR
dc.volume.number161
dspace.entity.typePublication
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relation.isAuthorOfPublication.latestForDiscovery0572736b-a8e3-40a1-9d3e-1654e35a7776
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