Effects of anti-estrogens on cell invasion and survival in pituitary adenoma cells: A systematic study

Hannen, Ricarda; Steffani, Marcella; Voellger, Benjamin; Carl, Barbara; Wang, Junwen; Bartsch, Jörg W.; Nimsky, Christopher

doi:10.1016/j.jsbmb.2018.11.005

Cited by 11 publications

(22 citation statements)

References 18 publications

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“…The impact of SERMs on viability and invasion in rodent PA cells and the correlation of MMP-14 and ADAM12 expression with invasiveness in human PAs have been demonstrated previously [4][5][6][7]13]. However, this is to our knowledge the first study that connects SERMs with reduced expression levels of MMP-14 and ADAM12, and reduced invasiveness in PA cell lines.…”

Section: Discussionmentioning

confidence: 59%

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Selective estrogen receptor modulators decrease invasiveness in pituitary adenoma cell lines AtT‐20 and TtT/GF by affecting expression of MMP‐14 and ADAM12

Zhang

Bartsch²,

Benzel³

et al. 2020

FEBS Open Bio

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Clinically, pituitary adenomas (PAs) become detrimental when invasive. We conducted an efficacy analysis of estrogen receptor modulators (SERMs) in PA cells. All SERMs blocked invasiveness of PA cells, correlating with expression levels of invasion‐related metalloproteases ADAM12 and MMP‐14. Our findings support the notion that SERMs are able to block invasiveness of PA cells by reducing their expression levels.

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Section: Discussionmentioning

confidence: 59%

“…Several in vitro studies suggest antitumorigenic effects of selective estrogen receptor modulators (SERMs) like resveratrol [4][5][6] or clinically applicable drugs like bazedoxifene, clomiphene, and raloxifene [7] on rodent PA cells. In acromegalic men, the SERM raloxifene has been shown to reduce insulin-like growth factor 1 levels [8].…”

mentioning

confidence: 99%

Selective estrogen receptor modulators decrease invasiveness in pituitary adenoma cell lines AtT‐20 and TtT/GF by affecting expression of MMP‐14 and ADAM12

Zhang

Bartsch²,

Benzel³

et al. 2020

FEBS Open Bio

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“…The invasion assay was executed as described previously [30]. Briefly, the percentage of the 25,000 seeded cells which invaded along an FCS gradient through the 8 µm pores of the transwell membrane into the matrigel was quantified.…”

Section: Methodsmentioning

confidence: 99%

“…To extract RNA, 50 mg tumor tissue was mechanically homogenized in 1 mL Qiazol (Qiagen, Hilden, Germany), whereas cells were lysed in 1 mL Qiazol by resuspending. The following steps were performed as previously described [30], including transcription to cDNA and qPCR.…”

Section: Methodsmentioning

confidence: 99%

Comparative Transcriptomic Analysis of Temozolomide Resistant Primary GBM Stem-Like Cells and Recurrent GBM Identifies Up-Regulation of the Carbonic Anhydrase CA2 Gene as Resistance Factor

Hannen

Selmansberger

Hauswald

et al. 2019

Cancers

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About 95% of patients with Glioblastoma (GBM) show tumor relapse, leaving them with limited therapeutic options as recurrent tumors are most often resistant to the first line chemotherapy standard Temozolomide (TMZ). To identify molecular pathways involved in TMZ resistance, primary GBM Stem-like Cells (GSCs) were isolated, characterized, and selected for TMZ resistance in vitro. Subsequently, RNA sequencing analysis was performed and revealed a total of 49 differentially expressed genes (|log2-fold change| > 0.5 and adjusted p-value < 0.1) in TMZ resistant stem-like cells compared to their matched DMSO control cells. Among up-regulated genes, we identified carbonic anhydrase 2 (CA2) as a candidate gene correlated with glioma malignancy and patient survival. Notably, we describe consistent up-regulation of CA2 not only in TMZ resistant GSCs on mRNA and protein level, but also in patient-matched clinical samples of first manifest and recurrent tumors. Co-treatment with the carbonic anhydrase inhibitor Acetazolamid (ACZ) sensitized cells to TMZ induced cell death. Cumulatively, our findings illustrate the potential of CA2 as a chemosensitizing target in recurrent GBM and provide a rationale for a therapy associated inhibition of CA2 to overcome TMZ induced chemoresistance.

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“…The molecular mechanisms underlying the generation of pituitary adenomas are largely unknown, but it is clear that estrogen plays an important role in their pathogenesis in both sexes [28]. In males, endogenous estradiol production requires aromatase (CYP19A1), a ubiquitous cytochrome P450 reductase enzyme, which catalyzes local tissue conversion of androgens to estrogens.…”

Section: Estrogen Signaling In the Anterior Pituitary And Prolactinommentioning

confidence: 99%

Pituitary Hyperplasia, Hormonal Changes and Prolactinoma Development in Males Exposed to Estrogens—An Insight From Translational Studies

Šošić‐Jurjević

Ajdžanović

Miljić

et al. 2020

IJMS

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Estrogen signaling plays an important role in pituitary development and function. In sensitive rat or mice strains of both sexes, estrogen treatments promote lactotropic cell proliferation and induce the formation of pituitary adenomas (dominantly prolactin or growth-hormone-secreting ones). In male patients receiving estrogen, treatment does not necessarily result in pituitary hyperplasia, hyperprolactinemia or adenoma development. In this review, we comprehensively analyze the mechanisms of estrogen action upon their application in male animal models comparing it with available data in human subjects. Sex-specific molecular targets of estrogen action in lactotropic (PRL) cells are highlighted in the context of their proliferative and secretory activity. In addition, putative effects of estradiol on the cellular/tumor microenvironment and the contribution of postnatal pituitary progenitor/stem cells and transdifferentiation processes to prolactinoma development have been analyzed. Finally, estrogen-induced morphological and hormone-secreting changes in pituitary thyrotropic (TSH) and adrenocorticotropic (ACTH) cells are discussed, as well as the putative role of the thyroid and/or glucocorticoid hormones in prolactinoma development, based on the current scarce literature.

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Effects of anti-estrogens on cell invasion and survival in pituitary adenoma cells: A systematic study

Cited by 11 publications

References 18 publications

Selective estrogen receptor modulators decrease invasiveness in pituitary adenoma cell lines AtT‐20 and TtT/GF by affecting expression of MMP‐14 and ADAM12

Selective estrogen receptor modulators decrease invasiveness in pituitary adenoma cell lines AtT‐20 and TtT/GF by affecting expression of MMP‐14 and ADAM12

Comparative Transcriptomic Analysis of Temozolomide Resistant Primary GBM Stem-Like Cells and Recurrent GBM Identifies Up-Regulation of the Carbonic Anhydrase CA2 Gene as Resistance Factor

Pituitary Hyperplasia, Hormonal Changes and Prolactinoma Development in Males Exposed to Estrogens—An Insight From Translational Studies

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