Soluble E-cadherin and IL-6 serum levels in patients affected by prostate cancer before and after prostatectomy

Sica, Gigliola

doi:10.3892/or.2012.1785

Cited by 8 publications

(4 citation statements)

References 26 publications

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“…Later, Kuefer et al [ 26 ] observed no difference between the expression of serum sE-cadherin in 61 men with localized PCa compared to controls. On the contrary, a more contemporary series also involving 61 patients with clinically localized PCa, reported by Iacopino et al [ 27 ], demonstrated serum sE-cadherin over-expression in PCa patients compared to that of healthy individuals, which is similar to our observation. However, no correlation of the marker with PSA, T-stage, GS, grade or R- and Pn-status was observed by those investigators.…”

Section: Discussionsupporting

confidence: 92%

sE-cadherin serves as a diagnostic and predictive parameter in prostate cancer patients

Tsaur

Thurn

Juengel

et al. 2015

J Exp Clin Cancer Res

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BackgroundMeasurement of prostate-specific antigen (PSA) advanced the diagnostic and prognostic potential for prostate cancer (PCa). However, due to PSA’s lack of specificity, novel biomarkers are needed to improve risk assessment and ensure optimal personalized therapy. A set of protein molecules as potential biomarkers was therefore evaluated in serum of PCa patients.MethodsSerum samples from patients undergoing radical prostatectomy (RPE) for biopsy-proven PCa without neoadjuvant treatment were compared to serum samples from healthy subjects. Preliminary screening of 119 proteins in 10 PCa patients and 10 controls was carried out by the Proteome Profiler Antibody Array. Those markers showing distinct differences between patients and controls were then further evaluated by ELISA in the serum of 165 PCa patients and 19 controls. Uni- and multivariate as well as correlation analysis were performed to test the capability of these molecules to detect disease and predict pathological outcome.ResultsScreening showed that soluble (s)E-cadherin, E-selectin, MMP2, MMP9, TIMP1, TIMP2, Galectin and Clusterin warranted further evaluation. sE-Cadherin, TIMP1, Galectin and Clusterin were significantly over- and MMP9 under-expressed in PCa compared to controls. The concentration of sE-cadherin, MMP2 and Clusterin correlated negatively and that of MMP9 and TIMP1 positively with the Gleason Sum at prostatectomy. Only sE-cadherin significantly correlated with the highest Gleason pattern. Compared to serum PSA, sE-cadherin provided an independent and better matching predictive ability for discriminating PCas with an upgrade at RPE and aggressive tumors with a Gleason Sum ≥7.ConclusionssE-cadherin performed most favorably from a large panel of serum proteins in terms of diagnostic and predictive potential in curatively treatable PCa. sE-cadherin merits further investigation as a biomarker for PCa.

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Section: Discussionsupporting

confidence: 92%

sE-cadherin serves as a diagnostic and predictive parameter in prostate cancer patients

Tsaur

Thurn

Juengel

et al. 2015

J Exp Clin Cancer Res

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“…IL-6 is known to be increased in patients with advanced stages of PCa (55, 56), play an important role in PCa progression (57), and can be secreted from several cell types, including macrophages (58) and adipocytes (59). In this study we found ECs are another source of IL-6.…”

Section: Discussionmentioning

confidence: 99%

Endothelial Cells Enhance Prostate Cancer Metastasis via IL-6→Androgen Receptor→TGF-β→MMP-9 Signals

Wang

Lee

Xia

et al. 2013

Molecular Cancer Therapeutics

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While the potential roles of endothelial cells (ECs) in the microvascules of prostate cancer (PCa) during angiogenesis have been documented, their direct impacts on the PCa metastasis remain unclear. We found that the CD31-positive and CD34-positive ECs are increased in PCa compared to the normal tissues and these ECs cells were decreased upon castration, gradually recovered with time, and become increased after PCa progresses into the castration resistant stage, suggesting a potential linkage of these ECs with androgen deprivation therapy. The in vitro invasion assays demonstrated that the co-culture of ECs with PCa cells significantly enhanced the invasion ability of the PCa cells. Mechanism dissection found that co-culture of PCa cells with ECs led to increased IL-6 secretion from ECs, which might result in down-regulation of AR signaling in PCa cells, and then the activation of TGF-β/MMP9 signaling. The consequences of the IL-6→androgen receptor→TGFβ→MMP9 signaling pathway might then trigger the increased invasion of PCa cells. Blocking the IL-6→androgen receptor→TGFβ→MMP9 signaling pathway either by IL-6 antibody, AR-siRNA, or TGF-β1 inhibitor all interrupted the ability of ECs to influence PCa invasion. These results, for the first time, revealed the important roles of ECs within the PCa microenvironment to promote the PCa metastasis, and provide new potential targets of IL-6→androgen receptor→TGFβ→MMP9 signals to battle the PCa metastasis.

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“…Interleukin-6 (IL-6) is a pleiotropic cytokine that stimulates proliferation and modulates key cellular events in prostate cancer [ 1 ]. The expression of IL-6 is elevated in advanced prostate cancer [ 2 ] and correlates with the Gleason grade of prostate cancer [ 3 ] and prostate cancer progression [ 4 ]. IL-6 is a major activator of the Janus kinase/signal transducer and activator of transcription 3 pathway in prostate cancer [ 5 ].…”

Section: Introductionmentioning

confidence: 99%

IL-6 Inhibits the Targeted Modulation of PDCD4 by miR-21 in Prostate Cancer

Dong

Shi²,

Wang

et al. 2015

PLoS ONE

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Prostate cancer is the most common cancer among men in the Unites States. The cytokine IL-6 activates several prostate cancer pathways, but its upstream trans-signaling pathway remains poorly understood. In this study, we evaluated the role of IL-6 in PDCD4 gene expression and how the microRNA miR-21 regulates this process in prostate cancer cell lines PC-3 and LNCaP. The expression pattern of PDCD4 from samples from human prostate cancer, precancerous lesions, and benign prostatic hyperplasia was investigated by immunohistochemistry. PDCD4 transcription and translation were detected by quantitative real-time PCR (qRT-PCR) and Western blot analysis, respectively. The targeted modulation of PDCD4 by miR-21 was analyzed in PC-3 and LNCaP cells, and the effect of IL-6 on the expression of PDCD4 was studied in vitro. PDCD4 expression in samples from the 3 tissue types progressively increased, and the expression levels of PDCD4 and prostate-specific antigen were negatively correlated. The levels of PDCD4 mRNA and protein in PC-3 and LNCaP cells transfected with anti–miR-21 constructs were lower than those in control cells. The expression of PDCD4 was inhibited by IL-6, but this effect was weakened in cell lines with low expression of miR-21. Our study demonstrates that the regulation of PDCD4 by miR-21 is targeted and IL-6 inhibits expression of the PDCD4 gene in PC-3 and LNCaP cells through the targeted function of miR-21 on PDCD4. These findings support the feasibility of future efforts for diagnosis and gene therapy for prostate cancer that are based on IL-6, miR-21, and PDCD4.

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Soluble E-cadherin and IL-6 serum levels in patients affected by prostate cancer before and after prostatectomy

Cited by 8 publications

References 26 publications

sE-cadherin serves as a diagnostic and predictive parameter in prostate cancer patients

sE-cadherin serves as a diagnostic and predictive parameter in prostate cancer patients

Endothelial Cells Enhance Prostate Cancer Metastasis via IL-6→Androgen Receptor→TGF-β→MMP-9 Signals

IL-6 Inhibits the Targeted Modulation of PDCD4 by miR-21 in Prostate Cancer

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