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IL-6, its receptors and its relationship with bcl-2 and bax proteins in infiltrating and in situ human breast carcinoma

Aims : To characterize the expression pattern of IL‐6 and its receptors (IL‐6Rα and gp130), to relate this pattern to bcl‐2 and bax expression and to elucidate the effects on the proliferation/apoptosis equilibrium in benign conditions and in situ and infiltrating breast cancer. Methods and results...

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Bibliographic Details
Published in:Histopathology 2005-07, Vol.47 (1), p.82-89
Main Authors: Garcia-Tuñón, I, Ricote, M, Ruiz, A, Fraile, B, Paniagua, R, Royuela, M
Format: Article
Language:English
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Summary:Aims : To characterize the expression pattern of IL‐6 and its receptors (IL‐6Rα and gp130), to relate this pattern to bcl‐2 and bax expression and to elucidate the effects on the proliferation/apoptosis equilibrium in benign conditions and in situ and infiltrating breast cancer. Methods and results : The immunoexpression of IL‐6 and its receptors (IL‐6Rα and gp130), and their relationship with bcl‐2 and bax proteins, were studied in in situ and infiltrating tumours and in benign breast lesions by means of Western blotting and immunohistochemistry. The percentages of samples positive for IL‐6, bcl‐2 and bax and their immunoreaction densities were higher in in situ carcinomas and infiltrating tumours than in benign lesions; although in in situ lesions were not so high as in infiltrating tumours, except for bax, whose immunoexpression was as weak as in benign conditions, resulting in a bcl‐2/bax ratio higher than in infiltrating tumours. Conclusions : The high expression of IL‐6 and its receptors in tumours might be related to the enhanced cell proliferation occurring in breast cancer. IL‐6 could act by increasing bcl‐2 expression and thus altering the proliferation/apoptosis balance toward neoplastic cell proliferation. The increased bax immunoreactivity observed only in infiltrating tumours, which was not so high as the increase in bcl‐2 immunoreactivity, might be interpreted as an attempt to hinder cell proliferation.
ISSN:0309-0167
1365-2559
DOI:10.1111/j.1365-2559.2005.02178.x