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      Low vitamin D status is associated with inflammation in patients with prostate cancer

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          Abstract

          Vitamin D deficiency has been associated with increased risks of prostate cancer. Nevertheless, the mechanisms remain unclear. The aim of this study was to analyze the association among prostate cancer, vitamin D status and inflammation. Sixty patients with newly diagnosed prostate cancer and 120 age-matched controls were recruited for this study. Vitamin D status was evaluated and serum inflammatory molecules were measured. Serum 25-(OH)D was lower in patients with prostate cancer. Moreover, serum 25(OH)D was lower in patients with severe prostate cancer than patients with mild and moderate prostate cancer. By contrast, serum C-reactive protein (CRP) and interleukin (IL)-8, two inflammatory molecules, were elevated in patients with prostate cancer. Serum 25-(OH)D was negatively correlated with serum CRP and IL-8 in patients with prostate cancer. Additional analysis showed that the percentage of vitamin D receptor positive nucleus in the prostate was reduced in patients with prostate cancer. By contrast, the percentage of nuclear factor kappa B p65-positive nucleus was elevated in patients with prostate cancer. Our results provide evidence that there is an association among prostate cancer, vitamin D deficiency and inflammatory signaling. Inflammation may be an important mediator for prostate cancer progression in patients with low vitamin D status.

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          The CXCL8-CXCR1/2 pathways in cancer

          Qian Liu, Anping Li, Yijun Tian … (2016)
          Persistent infection or chronic inflammation contributes significantly to tumourigenesis and tumour progression. C-X-C motif ligand 8 (CXCL8) is a chemokine that acts as an important multifunctional cytokine to modulate tumour proliferation, invasion and migration in an autocrine or paracrine manner. Studies have suggested that CXCL8 and its cognate receptors, C-X-C chemokine receptor 1 (CXCR1) and CX-C chemokine receptor 2 (CXCR2), mediate the initiation and development of various cancers including breast cancer, prostate cancer, lung cancer, colorectal carcinoma and melanoma. CXCL8 also integrates with multiple intracellular signalling pathways to produce coordinated effects. Neovascularisation, which provides a basis for fostering tumour growth and metastasis, is now recognised as a critical function of CXCL8 in the tumour microenvironment. In this review, we summarize the biological functions and ficlinical significance of the CXCL8 signalling axis in cancer. We also propose that CXCL8 may be a potential therapeutic target for cancer treatment
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            Interleukin-8 is a molecular determinant of androgen independence and progression in prostate cancer.

            Shinako Araki, Yohei Omori, Dominic Lyn … (2007)
            The proinflammatory chemokine interleukin-8 (IL-8) is undetectable in androgen-responsive prostate cancer cells (e.g., LNCaP and LAPC-4), but it is highly expressed in androgen-independent metastatic cells, such as PC-3. In this report, we show IL-8 functions in androgen independence, chemoresistance, tumor growth, and angiogenesis. We stably transfected LNCaP and LAPC-4 cells with IL-8 cDNA and selected IL-8-secreting (IL8-S) transfectants. The IL8-S transfectants that secreted IL-8 at levels similar to that secreted by PC-3 cells (100-170 ng/10(6) cells) were characterized. Continuous or transient exposure of LNCaP and LAPC-4 cells to IL-8 reduced their dependence on androgen for growth and decreased sensitivity (>3.5x) to an antiandrogen. IL-8-induced cell proliferation was mediated through CXCR1 and was independent of androgen receptor (AR). Quantitative PCR, immunoblotting, and transfection studies showed that IL8-S cells or IL-8-treated LAPC-4 cells exhibit a 2- to 3-fold reduction in PSA and AR levels, when compared with vector transfectants. IL8-S cells expressed 2- to 3-fold higher levels of phospho-EGFR, src, Akt, and nuclear factor kappaB (NF-kappaB) and showed increased survival when treated with docetaxel. This increase was blocked by NF-kappaB and src inhibitors, but not by an Akt inhibitor. IL8-S transfectants displayed a 3- to 5-fold increased motility, invasion, matrix metalloproteinase-9 and vascular endothelial growth factor production. LNCaP IL8-S cells grew rapidly as tumors, with increased microvessel density and abnormal tumor vasculature when compared with the tumors derived from their vector-transfected counterparts. Therefore, IL-8 is a molecular determinant of androgen-independent prostate cancer growth and progression.
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              Targeting the androgen receptor pathway in castration-resistant prostate cancer: progresses and prospects.

              R Ferraldeschi, J Welti, F. Luo … (2015)
              Androgen receptor (AR) signaling is a critical pathway for prostate cancer cells, and androgen-deprivation therapy (ADT) remains the principal treatment for patients with locally advanced and metastatic disease. However, over time, most tumors become resistant to ADT. The view of castration-resistant prostate cancer (CRPC) has changed dramatically in the last several years. Progress in understanding the disease biology and mechanisms of castration resistance led to significant advancements and to paradigm shift in the treatment. Accumulating evidence showed that prostate cancers develop adaptive mechanisms for maintaining AR signaling to allow for survival and further evolution. The aim of this review is to summarize molecular mechanisms of castration resistance and provide an update in the development of novel agents and strategies to more effectively target the AR signaling pathway.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Oncotarget
                Journal ID (iso-abbrev): Oncotarget
                Journal ID (publisher-id): Oncotarget
                Journal ID (publisher-id): ImpactJ
                Title: Oncotarget
                Publisher: Impact Journals LLC
                ISSN (Electronic): 1949-2553
                Publication date Collection: 28 March 2017
                Publication date (Electronic): 15 March 2017
                Volume: 8
                Issue: 13
                Pages: 22076-22085
                Affiliations
                1 Department of Urology, Second Affiliated Hospital, Anhui Medical University, Hefei 230022, China
                2 Department of Toxicology, Anhui Medical University, Hefei 230032, China
                3 Department of Histology and Embryology, Anhui Medical University, Hefei 230032, China
                4 Life Science College, Anhui Medical University, Hefei 230032, China
                Author notes
                Correspondence to: De-Xin Yu, yudx_urology@ 123456126.com
                De-Xiang Xu, xudex@ 123456126.com
                Article
                Publisher ID: 16195
                DOI: 10.18632/oncotarget.16195
                PMC ID: 5400647
                PubMed ID: 28423553
                SO-VID: 94e698e3-3a2f-46f9-bd0a-280d93acb0a5
                Copyright © Copyright: © 2017 Xie et al.
                License:

                This article is distributed under the terms of the Creative Commons Attribution License (CC-BY), which permits unrestricted use and redistribution provided that the original author and source are credited.

                History
                Date received : 10 November 2016
                Date accepted : 22 January 2017
                Categories
                Subject: Research Paper

                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: prostate cancer,vitamin d deficiency,inflammation,vitamin d receptor,nuclear factor kappa b p65
                Data availability:
                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: prostate cancer, vitamin d deficiency, inflammation, vitamin d receptor, nuclear factor kappa b p65

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