Letrozole Decreased Testosterone-Induced Cell Proliferation and Prolactin Secretion also Increased Apoptosis in MMQ and GH3 Rat Prolactinoma Cell Lines

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dc.authorid0000-0002-9926-369X
dc.authorid0000-0001-6814-0585
dc.authorid0000-0002-9992-833X
dc.contributor.authorSelek, Alev
dc.contributor.authorHalbutogullari, Zehra Seda Unal
dc.contributor.authorAydemir, Cigdem Inci
dc.contributor.authorCetinarslan, Berrin
dc.contributor.authorCanturk, Zeynep
dc.contributor.authorTarkun, Ilhan
dc.contributor.authorErdal, Karaoz
dc.date.accessioned2026-02-12T21:05:04Z
dc.date.available2026-02-12T21:05:04Z
dc.date.issued2023
dc.departmentBursa Teknik Üniversitesi
dc.description.abstractAromatase enzyme plays an essential role in estrogen-induced tumorigenesis. It is expressed in the normal pituitary and more significantly in prolactinoma tissues. The aim of this study was to investigate the effects of an aromatase inhibitor, letrozole, on MMQ and GH3 rat prolactinoma cell lines and evaluate the possible mechanism of action. MMQ and GH3 cells were characterized with demonstrating aromatase enzyme and estrogen receptor alpha expression by PCR and immunofluorescence staining. After dose optimization for testosterone (T) and letrozole (L), four groups were established: only the testosteron-treated group (T) to detect cell proliferation; only letrozole-treated group (L) to investigate apoptotic effects; testosterone and letrozole concomitant-treated group to demonstrate inhibition of testosterone induced cell proliferation with letrozole treatment s(T + L) and control group (C) with no treatment. The proliferation rate of cells was determined by WST-1. For the detection of apoptotic and necrotic cells, Annexin V and caspase-3 labeling was used. Prolactin and estrogen levels were measured with ELISA, and the mRNA expression of aromatase and Esr1 was also determined. Testosterone induced the proliferation of MMQ and GH3 cells and further increased prolactin and estradiol levels. Adding letrozole to testosterone resulted in decreased cellular proliferation and even induced apoptosis. Also, letrozole administration significantly decreased prolactin and estradiol levels. However, letrozole alone had no effects on proliferation and apoptosis. Gene expression of aromatase and Esr1 was also significantly decreased by letrozole treatment. This in vitro study demonstrated that treatment of testosterone proliferating cells with letrozole resulted in decreased prolactin levels and cell proliferation and induced apoptosis, and further loss of aromatase and Esr1 mRNA expression were observed. Although this is an in vivo study, the results showed unique and novel findings which may easily be adapted to clinical use for further verification.
dc.description.sponsorshipResearch Fund of the University; Novo-Nordisk collaboration [2013/155]
dc.description.sponsorshipThe study was supported by the Research Fund of the University and Novo-Nordisk collaboration, project no. 2013/155.
dc.identifier.doi10.1007/s12035-023-03220-2
dc.identifier.endpage2454
dc.identifier.issn0893-7648
dc.identifier.issn1559-1182
dc.identifier.issue5
dc.identifier.pmid36662360
dc.identifier.scopus2-s2.0-85146550270
dc.identifier.scopusqualityQ1
dc.identifier.startpage2442
dc.identifier.urihttps://doi.org/10.1007/s12035-023-03220-2
dc.identifier.urihttps://hdl.handle.net/20.500.12885/6757
dc.identifier.volume60
dc.identifier.wosWOS:000920536900001
dc.identifier.wosqualityQ1
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherSpringer
dc.relation.ispartofMolecular Neurobiology
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.snmzKA_WoS_20260212
dc.subjectAromatase
dc.subjectProlactinoma
dc.subjectAromatase inhibitors
dc.subjectEstrogen receptor
dc.subjectProlactin
dc.titleLetrozole Decreased Testosterone-Induced Cell Proliferation and Prolactin Secretion also Increased Apoptosis in MMQ and GH3 Rat Prolactinoma Cell Lines
dc.typeArticle

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