ECE2016 Eposter Presentations Thyroid cancer (81 abstracts)
Visualization of kallikreins in thyroid epithelial and carcinoma cells
Eileen Kroll 1 , Anastasija Pejkovska 1 , Maren Rehders 1 , Adam Lesner 2 , Grzegorz Dubin 3 , Tomasz Kantyka 3 , Dagmar Führer 4 , Jan Potempa 3 & Klaudia Brix 1
1Department of Life Sciences and Chemistry, Jacobs University Bremen, Bremen, Germany; 2Department of Biochemistry, Faculty of Chemistry, University of Gdansk, Gdansk, Poland; 3Faculty of Biochemistry, Biophysics and Biotechnology, Jagiellonian University, Krakow, Poland; 4Klinik für Endokrinologie & Stoffwechselerkrankungen und Zentrallabor, Universitätsklinikum Essen, Essen, Germany.
Human tissue kallikreins (KLKs) are serine proteases expressed in various organs including thyroid hormone-generating and target tissues. Besides their involvement in important physiological processes, KLKs are mainly recognized for their association with pathological conditions like cancer. Previously, KLK2 and KLK3 transcripts were detected in normal thyroid and carcinoma tissue, while the levels and subcellular distribution of KLK proteins remained largely elusive. Since the thyroid gland is a hormonally regulated organ, we were interested in investigating possible changes of KLK levels and localization in thyroid epithelial and carcinoma cells upon stimulation with the thyroid stimulating hormone (TSH). The results revealed a redistribution of KLK2 and KLK3 from centrally to peripherally located vesicles upon TSH stimulation of thyroid epithelial cells, indicating TSH-regulated trafficking of KLKs in normal thyrocytes. Moreover, KLK2 and KLK3 were localized to the nuclei of thyroid carcinoma cells, but they were not detectable at this unexpected subcellular localization in thyroid epithelial cells. Thus, KLKs might contribute to thyroid carcinogenesis in different ways, i.e. by their enhanced expression and thus altered protein homeostasis, and by proteolytically processing nuclear substrates which are involved in the regulation of cell cycle progression.
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Endocrine Abstracts
ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
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