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      Paradoxical Roles of Tumour Necrosis Factor-Alpha in Prostate Cancer Biology

      review-article
      Author(s): 1 , 2 , 3 , 1 , 2 , *
      Publication date (Electronic):
      Journal: Prostate Cancer
      Publisher: Hindawi Publishing Corporation

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          Abstract

          Tumour necrosis factor (TNF) is a pleiotropic cytokine with dual roles in cancer biology including prostate cancer (PCa). On the one hand, there is evidence that it stimulates tumour angiogenesis, is involved in the initiation of PCa from an androgen-dependent to a castrate resistant state, plays a role in epithelial to mesenchymal plasticity, and may contribute to the aberrant regulation of eicosanoid pathways. On the other hand, TNF has also been reported to inhibit neovascularisation, induce apoptosis of PCa cells, and stimulate antitumour immunity. Much of the confusion surrounding its seemingly paradoxical roles in cancer biology stems from the dependence of its effects on the biological model within which TNF is investigated. This paper will address some of these issues and also discuss the therapeutic implications.

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          An endotoxin-induced serum factor that causes necrosis of tumors.

          E. A. Carswell, L Old, R. L. Kassel … (1975)
          In studying "hemorrhagic necrosis" of tumors produced by endotoxin, it was found that the serum of bacillus Calmette--Guerin (BCG)-infected mice treated with endotoxin contains a substance (tumor necrosis factor; TNF) which mimics the tumor necrotic action of endotoxin itself. TNF-positive serum is as effective as endotoxin itself in causing necrosis of the sarcoma Meth A and other transplanted tumors. A variety of tests indicate that TNF is not residual endotoxin, but a factor released from host cells, probably macrophages, by endotoxin. Corynebacteria and Zymosan, which like BCG induce hyperplasia of the reticulo-endothelial system, can substitute for BCG in priming mice for release of TNF by endotoxin. TNF is toxic in vitro for two neoplastic cell lines; it is not toxic for mouse embryo cultures. We propose that TNF mediates endotoxin-induced tumor necrosis, and that it may be responsible for the suppression of transformed cells by activated macrophages.
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            Tumor necrosis factor and cancer, buddies or foes?

            Xia Wang, Chen-Yong Lin (2008)
            Tumor necrosis factor (TNF) is a multifunctional cytokine that plays important roles in diverse cellular events such as cell survival, proliferation, differentiation, and death. As a pro-inflammatory cytokine, TNF is secreted by inflammatory cells, which may be involved in inflammation-associated carcinogenesis. TNF exerts its biological functions through activating distinct signaling pathways such as nuclear factor-kappaB (NF-kappaB) and c-Jun N-terminal kinase (JNK). NF-kappaB is a major cell survival signal that is anti-apoptotic, whereas sustained JNK activation contributes to cell death. The crosstalk between the NF-kappaB and JNK is involved in determining cellular outcomes in response to TNF. In regard to cancer, TNF is a double-dealer. On one hand, TNF could be an endogenous tumor promoter, because TNF stimulates the growth, proliferation, invasion and metastasis, and tumor angiogenesis of cancer cells. On the other hand, TNF could be a cancer killer. The property of TNF in inducing cancer cell death renders it a potential cancer therapeutic, although much work is needed to reduce its toxicity for systematic TNF administration. Recent studies have focused on sensitizing cancer cells to TNF-induced apoptosis through inhibiting survival signals such as NF-kappaB, by combined therapy. In this article we provide an overview of the roles of TNF-induced signaling pathways in cancer biology with specific emphasis on carcinogenesis and cancer therapy.
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              Androgen levels increase by intratumoral de novo steroidogenesis during progression of castration-resistant prostate cancer.

              Jennifer Locke, Emma S Guns, Amy A. Lubik … (2008)
              Although systemic androgen deprivation prolongs life in advanced prostate cancer, remissions are temporary because patients almost uniformly progress to a state of a castration-resistant prostate cancer (CRPC) as indicated by recurring PSA. This complex process of progression does not seem to be stochastic as the timing and phenotype are highly predictable, including the observation that most androgen-regulated genes are reactivated despite castrate levels of serum androgens. Recent evidence indicates that intraprostatic levels of androgens remain moderately high following systemic androgen deprivation therapy, whereas the androgen receptor (AR) remains functional, and silencing the AR expression following castration suppresses tumor growth and blocks the expression of genes known to be regulated by androgens. From these observations, we hypothesized that CRPC progression is not independent of androgen-driven activity and that androgens may be synthesized de novo in CRPC tumors leading to AR activation. Using the LNCaP xenograft model, we showed that tumor androgens increase during CRPC progression in correlation to PSA up-regulation. We show here that all enzymes necessary for androgen synthesis are expressed in prostate cancer tumors and some seem to be up-regulated during CRPC progression. Using an ex vivo radiotracing assays coupled to high-performance liquid chromatography-radiometric/mass spectrometry detection, we show that tumor explants isolated from CRPC progression are capable of de novo conversion of [(14)C]acetic acid to dihydrotestosterone and uptake of [(3)H]progesterone allows detection of the production of six other steroids upstream of dihydrotestosterone. This evidence suggests that de novo androgen synthesis may be a driving mechanism leading to CRPC progression following castration.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Prostate Cancer
                Journal ID (iso-abbrev): Prostate Cancer
                Journal ID (publisher-id): PC
                Title: Prostate Cancer
                Publisher: Hindawi Publishing Corporation
                ISSN (Print): 2090-3111
                ISSN (Electronic): 2090-312X
                Publication date (Print): 2012
                Publication date (Electronic): 27 December 2012
                Volume: 2012
                Electronic Location Identifier: 128965
                Affiliations
                1Australian Prostate Cancer Research Centre-Queensland, Queensland University of Technology, Brisbane, QLD 4102, Australia
                2Institute of Health and Biomedical Innovation, Cells and Tissue Domain, Faculty of Health, Queensland University of Technology, Brisbane, QLD 4059, Australia
                3Department of Medicine, St. George Hospital Clinical School, The University of New South Wales, Sydney, NSW 2217, Australia
                Author notes

                Academic Editor: Jostein Halgunset

                Article
                DOI: 10.1155/2012/128965
                PMC ID: 3543804
                PubMed ID: 23326670
                SO-VID: 7b767ecf-0776-4408-990e-df4d327c1eb1
                Copyright © Copyright © 2012 Brian W. C. Tse et al.
                License:

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 26 September 2012
                Date accepted : 19 November 2012
                Categories
                Subject: Review Article

                ScienceOpen disciplines: Oncology & Radiotherapy
                Data availability:
                ScienceOpen disciplines: Oncology & Radiotherapy

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