Startseite Novel expression of kallikreins, kallikrein-related peptidases and kinin receptors in human pleural mesothelioma
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Novel expression of kallikreins, kallikrein-related peptidases and kinin receptors in human pleural mesothelioma

  • Jessica Chee , Jasmine Singh , Anupam Naran , Neil L. Misso , Philip J. Thompson und Kanti D. Bhoola
Veröffentlicht/Copyright: 2. November 2007
Biological Chemistry
Aus der Zeitschrift Band 388 Heft 11

Abstract

Malignant mesothelioma is an aggressive cancer of the pleura that is causally related to exposure to asbestos fibres. The kallikrein serine proteases [tissue (hK1) and plasma (hKB1) kallikreins, and kallikrein-related peptidases (KRP/hK2–15)] and the mitogenic kinin peptides may have a role in tumourigenesis. However, it is not known whether hK1, hKB1, KRP/hK proteins or kinin receptors are expressed in pleural mesotheliomas. The expression of hK1, hKB1, KRP/hK2, 5, 6, 7, 8 and 9, and kinin B1 and B2 receptors was assessed in archived selected normal tissue and mesothelioma tumour sections by immunoperoxidase and immunofluorescence labelling. hK1, hKB1 and kinin B1 and B2 receptors were expressed in malignant cells of the epithelioid and sarcomatoid components of biphasic mesothelioma tumour cells. The percentage of cells with cytoplasmic and nuclear labelling and the intensity of labelling were similar for hK1, hKB1 and the kinin receptors. KRP/hK2, 6, 8 and 9 were also expressed in the cytoplasm and nuclei of mesothelioma cells, whereas KRP/hK5 and hK7 showed predominantly cytoplasmic localisation. This is a first report, but further studies are required to determine whether these proteins have a functional role in the pathogenesis of mesothelioma and/or may be potential biomarkers for pleural mesothelioma.


Corresponding author

Received: 2007-4-26
Accepted: 2007-7-5
Published Online: 2007-11-02
Published in Print: 2007-11-01

©2007 by Walter de Gruyter Berlin New York

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Heruntergeladen am 21.11.2025 von https://www.degruyterbrill.com/document/doi/10.1515/BC.2007.139/html
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