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BMC Cancer

, 10:385

First Online: 21 July 2010Received: 18 January 2010Accepted: 21 July 2010DOI: 10.1186-1471-2407-10-385

Cite this article as: Monsef, N., Soller, M., Panagopoulos, I. et al. BMC Cancer 2010 10: 385. doi:10.1186-1471-2407-10-385

Abstract

BackgroundNeuroendocrine NE differentiation in prostate cancer has been correlated with a poor prognosis and hormone refractory disease. In a previous report, we demonstrated the presence of immunoreactive cytoplasmic hypoxia inducible factor 1α HIF1α, in both benign and malignant NE prostate cells. HIF1α and HIF1β are two subunits of HIF1, a transcription factor important for angiogenesis. The aim of this study was to elucidate whether the cytoplasmic stabilization of HIF1α in androgen independent NE differentiated prostate cancer is due to the presence of certain HIF1α isoforms.

MethodsWe studied the HIF1α isoforms present in 8 cases of benign prostate hyperplasia BPH and 43 cases of prostate cancer with and without NE differentiation using RT-PCR, sequencing analysis, immunohistochemistry and in situ hybridization.

ResultsWe identified multiple isoforms in both benign and malignant prostate tissues. One of these isoforms, HIF1α1.2, which was previously reported to be testis specific, was found in 86% of NE-differentiated prostate tumors, 92% of HIF1α immunoreactive prostate tumors and 100% of cases of benign prostate hyperplasia. Immunohistochemistry and in situ hybridization results showed that this isoform corresponds to the cytoplasmic HIF1α present in androgen-independent NE cells of benign and malignant prostate tissue and co-localizes with immunoreactive cytoplasmic HIF1β.

ConclusionOur results indicate that the cytoplasmic stabilization of HIF1α in NE-differentiated cells in benign and malignant prostate tissue is due to presence of an HIF1α isoform, HIF1α1.2. Co-localization of this isoform with HIF1β indicates that the HIF1α1.2 isoform might sequester HIF1β in the cytoplasm.

Electronic supplementary materialThe online version of this article doi:10.1186-1471-2407-10-385 contains supplementary material, which is available to authorized users.

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Autor: Nastaran Monsef - Maria Soller - Ioannis Panagopoulos - Per Anders Abrahamsson

Fuente: https://link.springer.com/







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