Expression of Transglutaminase K in Normal Cervix Tissue and Cervix Carcinomas |
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Authors: | Michael Friedrich, Carlos Villena-Heinsen, Jianping He, Dieter Mink, Jö rg Reichrath, Karin Reitnauer Werner Schmidt |
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Affiliation: | (1) Department of Gynecology, University of the Saarland, D-66421 Homburg/Saar, Germany;(2) Department of Dermatology, University of the Saarland, D-66421 Homburg/Saar, Germany;(3) Department of Pathology, University of the Saarland, D-66421 Homburg/Saar, Germany |
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Abstract: | The localization and expression of transglutaminase K has been investigated immunohistochemically in normal cervix tissue (n=15) and in cervix carcinomas (n=23). The distribution of the transglutaminase K was compared with the staining patterns of cytokeratin 10, Ki-67, p53, and oestrogen and progesterone receptors in these tumours. Weak to strong membrane-bound immunoreactivity for transglutaminase K was detected in almost all cervix carcinomas analyzed. The immunostaining was heterogeneous, with visual differences between individual tumour cells. 66.7% of normal cervix tissues revealed no immunoreactivity for the transglutaminase K. In normal cervix tissue, the immunoreactivity was confined to upper cervix layers, predominantly to the superficial and intermediate cell layers. The intensity of both the immunostaining and the number of transglutaminase K-positive cells were upregulated in cervix carcinomas as compared to normal cervix tissue. When the coexpressions of transglutaminase K with markers of proliferation and differentiation were analyzed, no statistically significant correlation was found. Our findings indicate that (1) transglutaminase K is upregulated at the protein level in cervix carcinomas as compared to normal cervix tissue; (2) upregulation of the transglutaminase K in cervix carcinoma is not exclusively induced by alterations of epithelial differentiation or proliferation, but by different, unknown mechanisms; and (3) upregulation of transglutaminase K in cervix carcinomas may play an important role for the regulation of tumour invasive properties by modulating cell–cell interactions. |
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