Open Access Highly Accessed Research article

Role of IAPs in prostate cancer progression: immunohistochemical study in normal and pathological (benign hyperplastic, prostatic intraepithelial neoplasia and cancer) human prostate

Gonzalo Rodríguez-Berriguete1, Benito Fraile1, Fermín R de Bethencourt3, Angela Prieto-Folgado1, Nahikari Bartolome1, Claudia Nuñez1, Bruna Prati1, Pilar Martínez-Onsurbe2, Gabriel Olmedilla2, Ricardo Paniagua1 and Mar Royuela1*

Author Affiliations

1 Department of Cell Biology and Genetics. University of Alcalá; 28871 Alcalá de Henares. Madrid, Spain

2 Department of Pathology, Príncipe de Asturias Hospital. 28806 Alcalá de Henares. Madrid, Spain

3 Department of Urology, "La Paz" Hospital. Madrid, Spain

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BMC Cancer 2010, 10:18  doi:10.1186/1471-2407-10-18

Published: 15 January 2010



In this study was investigate IAPs in normal human prostate (NP), benign prostatic hyperplasia (BPH), prostatic intraepithelial neoplasia (PIN) and prostatic carcinoma (PC), and their involvement in apoptosis/proliferation via NF-kB (TNF-α, IL-1) stimulation.


Immunohistochemical and Western blot analyses were performed in 10 samples of normal prostates, 35 samples of BPH, 27 samples diagnosis of PIN (with low-grade PIN or high-grade PIN) and 95 samples of PC (with low, medium or high Gleason grades).


In NP, cytoplasm of epithelial cells were positive to c-IAP1/2 (80% of samples), c-IAP-2 (60%), ILP (20%), XIAP (20%); negative to NAIP and survivin. In BPH, epithelial cells were immunostained to c-IAP1/2 (57.57%), c-IAP-2 (57.57%), ILP (66.6%), NAIP (60.6%), XIAP (27.27%), survivin (9.1%). Whereas low-grade PIN showed intermediate results between NP and BPH; results in high-grade PIN were similar to those found in PC. In PC, epithelial cells were immunostained to c-IAP1/2, c-IAP-2, ILP, NAIP, XIAP (no Gleason variation) and survivin (increasing with Gleason).


IAPs could be involved in prostate disorder (BPH, PIN and PC) development since might be provoke inhibition of apoptosis and subsequently cell proliferation. At the same time, different transduction pathway such as IL-1/NIK/NF-kB or TNF/NF-kB (NIK or p38) also promotes proliferation. Inhibitions of IAPs, IL-1α and TNFα might be a possible target for PC treatment since IAPs are the proteins that inhibited apoptosis (favour proliferation) and IL-1α and TNFα would affect all the transduction pathway involucrate in the activation of transcription factors related to survival or proliferation (NF-kB, Elk-1 or ATF-2).