Clinical significance of serum angiocidin levels in hepatocellular carcinoma

Sabherwal, Yamini; Rothman, Vicki L.; Poon, Ronnie Tung‐Ping; Tuszynski, George P.

doi:10.1016/j.canlet.2006.10.023

Cited by 10 publications

(12 citation statements)

References 14 publications

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“…During their differentiation, the cells became flattened, elongated and firmly attached to the tissue culture plastic. Earlier reports have indicated the presence of angiocidin in tumor-conditioned medium and in the serum of cancer patients (Sabherwal et al, 2007). Because of the high sequence similarity between angiocidin and S5a, we postulated that these proteins could share a similar function, inducing THP-1 adhesion and/or differentiation.…”

Section: Resultsmentioning

confidence: 82%

“…Recent studies have reported that S5a/angiocidin inhibits endothelial cell proliferation and induces endothelial cell apoptosis and antitumor activities that are related to the activity of polyubiquitin conjugates (Saeki and Tanaka, 2008). Restructuring angiocidin offers a variety of mechanisms for antitumor activity in vitro and in vivo (Sabherwal et al, 2007;L'Heureux et al, 2010;Liebig et al, 2009;Kremlev et al, 2008;Yang et al, 2006). In this study, we focused on another aspect of the antitumor activity of S5a, by inducing the differentiation of THP-1 cells into macrophages.…”

Section: Endogenous S5a Is a Crucial Protein For Monocyte Self-regulamentioning

confidence: 99%

“…Researchers have been able to detect angiocidin in tumorconditioned medium and in the serum of cancer patients (Sabherwal et al, 2007). As the protein sequence of angiocidin has a high degree of similarity to that of S5a, we hypothesized that THP-1 cells released endogenous S5a, which then induced companion and neighboring cells to differentiate.…”

Section: Introductionmentioning

confidence: 99%

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S5a binds death receptor-6 to induce THP-1 monocytes differentiation via NF-κB pathway

Wang

Fan

Zhou

et al. 2014

Journal of Cell Science

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Analyses of supernatants from apoptotic cells have helped in the identification of many signals that modulate the states of cell activation and differentiation. However, the current knowledge about the soluble factors that are released during apoptosis is rather limited. Previous studies have shown that S5a and angiocidin (both encoded by PSMD4) induce human acute monocytic leukemia cells (THP-1 cells) to differentiate into macrophages, but the cell-surface receptor of S5a has not been identified. In this study, we show that apoptotic THP-1 cells release endogenous S5a that binds to death receptor-6 (DR6, also known as TNFRSF1), which was identified as an orphan receptor, to induce THP-1 cells to differentiate. Furthermore, we found that the NF-kB pathway is activated, and that the transcription factors WT1 (Wilms' tumor 1) and c-myb mediate S5a-induced THP-1 differentiation. We also show that differentiation is blocked by anti-DR6 antibody, DR6 siRNA, DR6-Fc, NF-kB inhibitor or WT1 siRNA treatment. Our findings indicate that the interaction between cells can determine their differentiation, and we provide evidence for a functional interaction between S5a and DR6, which provides a novel potential mechanism to induce the differentiation of cancer cells, especially during biotherapy for leukemia.

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Section: Resultsmentioning

confidence: 82%

Section: Endogenous S5a Is a Crucial Protein For Monocyte Self-regulamentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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S5a binds death receptor-6 to induce THP-1 monocytes differentiation via NF-κB pathway

Wang

Fan

Zhou

et al. 2014

Journal of Cell Science

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“…Colon cancer cells expressing low-level angiocidin exhibited very low proliferation rates than high expression cells. In vivo, nude mice injected with low angiocidin expression colon cancer cells develop significantly smaller tumors than the mice injected with normal cells [8][9][10][11][12] . These above results suggest that angiocidin may play a key role in tumor growth.…”

Section: Introductionmentioning

confidence: 99%

Reduction of angiocidin contributes to decreased HepG2 cell proliferation

Guan

Guan²,

Feng³

et al. 2013

Afr H. Sci.

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Background: Angiocidin plays a key role in angiogenesis and tumor progression. High angiocidin expression is detected in some kind of solid tumors and tumor vascular endothelial cells. Several reports have shown the inhibition of angiogenesis and tumor growth caused by angiocidin. However, the role of angiocidin in liver cancers growth is still unclear. Objectives: To examine angiocidin expression in SMMC-7221 and HepG2 cells and the role of angiocidin in liver cancer cell growth. Methods: RT-PCR and western blot are used in this study to detect angiocidin expression. SiRNA and MTT experiments are used in exploring the role of angiocidin in tumor cell growth. Results: Our study showed high angiocidin expression in two kinds of liver cancer cells. Angiocidin protein production in HepG2 cells were reduced significantly by siRNA. When HepG2 cells were transfected with siRNA-angiocidin, these cells showed very low proliferation activity compared with control cells. Our study suggests that reduction of angiocidin may contribute to decreased proliferation activity in liver cancer cells. Conclusion: Angiocidin is highly expressed in liver cancer cells, and it may play a key role in tumor growth of liver cancers.

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“…8,9 Overexpression of angiocidin has been shown in many solid epithelial tumors, and increased levels of angiocidin have been demonstrated in the serum of patients with different epithelial malignancies. 10,11 Preliminary reports have shown low to negligible expression of angiocidin in normal adult tissues, making it an attractive molecular target for tumor-specific therapy. 9,12,13 The protumor effects of angiocidin are the result of highaffinity binding interactions with extracellular matrix proteins including thrombospondin-1 (TSP-1), a matrix protein produced in tumors by activated stromal cells of mesenchymal origin.…”

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confidence: 99%

The role of angiocidin in sarcomas

Liebig

Wilks

Feig

et al. 2009

Cancer

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We investigated growth kinetics of microalgae, Chlorella vulgaris, in immobilized arrays of nanoliter‐scale microfluidic drops. These static drop arrays enabled simultaneous monitoring of growth of single as well as multiple cells encapsulated in individual droplets. To monitor the growth, individual drop volumes were kept nearly intact for more than a month by controlling the permeation of water in and out of the microfluidic device. The kinetic growth parameters were quantified by counting the increase in the number of cells in each drop over time. In addition to determining the kinetic parameters, the cell‐size distribution of the microalgae was correlated with different stages of the growth. The single‐cell growth kinetics of C. vulgaris showed significant heterogeneity. The specific growth rate ranged from 0.55 to 1.52 day−1 for different single cells grown in the same microfluidic device. In comparison, the specific growth rate in bulk‐scale experiment was 1.12 day−1. It was found that the average cell size changes significantly at different stages of the cell growth. The mean cell‐size increased from 5.99 ± 1.08 to 7.33 ± 1.3 µm from exponential to stationary growth phase. In particular, when multiple cells are grown in individual drops, we find that in the stationary growth phase, the cell size increases with the age of cell suggesting enhanced accumulation of fatty acids in older cells. Biotechnol. Bioeng. 2012; 109: 2987–2996. © 2012 Wiley Periodicals, Inc.

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Clinical significance of serum angiocidin levels in hepatocellular carcinoma

Cited by 10 publications

References 14 publications

S5a binds death receptor-6 to induce THP-1 monocytes differentiation via NF-κB pathway

S5a binds death receptor-6 to induce THP-1 monocytes differentiation via NF-κB pathway

Reduction of angiocidin contributes to decreased HepG2 cell proliferation

The role of angiocidin in sarcomas

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