Chondroitin sulfate A chains enhance platelet derived growth factor-mediated signalling in fibrosarcoma cells

Fthenou, Eleni; Zafiropoulos, Alexandros; Tsatsakis, Aristidis; Stathopoulos, Apostolos; Karamanos, Nikos K.; Tzanakakis, George N.

doi:10.1016/j.biocel.2006.06.006

Cited by 29 publications

(34 citation statements)

References 36 publications

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“…Platelet-derived growth factors (PDGFs) are involved in regulating proliferation of cancer cells and stimulating tumor angiogenesis, and chondroitin sulfate has been shown to enhance PDGF action by enhancing signaling of the tyrosine kinase receptors. 34 Indeed, PDGF and its receptor have been reported to be upregulated in prostate adenocarcinoma, and expression of PDGF receptor has been shown to mark prostate cancer cells with the greatest disposition for bony metastasis. 35,36 Stromal cell-derived factor-1 (SDF-1) is a chemoattractant for prostate carcinoma cells.…”

Section: Discussionmentioning

confidence: 99%

Increased expression of non-sulfated chondroitin correlates with adverse clinicopathological parameters in prostate cancer

et al. 2008

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Chondroitin sulfate is a structurally diverse glycosaminoglycan, which contains a variable degree of sulfation that helps to determine its biological function. It is involved in the regulation of cellular activity and has been implicated in carcinogenesis. To determine if the non-sulfated chondroitin backbone has a functional role in prostate cancer, we analyzed its expression by immunohistochemistry using the 1B5 monoclonal antibody and a set of tissue microarrays constructed with 227 prostate specimen cores from 81 cases of benign prostate tissue and 77 cases of prostate cancer, of which 69 of these cases are matched. Non-sulfated chondroitin was found in the secretory epithelial cells and stromal regions of both prostatic adenocarcinoma and benign prostatic tissues, as well as in the basal cells of benign glands. A higher percentage of cancerous cells were stained positively for non-sulfated chondroitin as compared with benign secretory cells of the same patient. Cancerous cells stained more intensely for non-sulfated chondroitin. This increase in percentage of cells stained and increase in staining intensity were associated with higher pathological T stage and extraprostatic extension. Non-sulfated chondroitin expression (either staining intensity or percentage of cells stained) in adenocarcinoma and its peritumoral stroma correlated significantly with several clinicopathological parameters of unfavorable outcome, including higher pathological T stage and Gleason score, presence of tumor in both prostatic lobes, extraprostatic extension, seminal vesicle involvement and preoperative prostate-specific antigen levels. These data suggest that non-sulfated chondroitin is a potentially useful biomarker for prostate cancer, and may be involved in regulating prostate cancer behavior.

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Section: Discussionmentioning

confidence: 99%

Increased expression of non-sulfated chondroitin correlates with adverse clinicopathological parameters in prostate cancer

et al. 2008

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“…Exogenously added CS-A combined with PDGF showed a positive synergistic effect on the growth of fibrosarcoma cells, in vitro. It was put forward that this co-stimulatory effect of CS-A and PDGF was due to more efficient signaling [48]. Clearly, the effect of CS on the binding and signaling effect of growth factors is complicated and likely dependent on the CS fine structure.…”

Section: Tumor Angiogenesismentioning

confidence: 98%

Sulfated sugars in the extracellular matrix orchestrate ovarian cancer development: ‘When sweet turns sour’

Vallen

Steen

Tilborg

et al. 2014

Gynecologic Oncology

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“…PDGF has been shown to physically interact with GAGs, which are abundant in the fibrosarcoma cell microenvironment and regulate the growth of fibrosarcoma cell lines (Fager et al, 1995;Fthenou et al, 2006). In more detail, Fthenou et al have demonstrated significant co-stimulatory effects of chondroitin sulfate A and PDGF-BB in the modulation of the growth of HT1080 and B6FS fibrosarcoma cell lines (Fthenou et al, 2006). This co-stimulatory effect was perpetrated through more efficient signaling of tyrosine kinase receptors (Fthenou et al, 2006).…”

Section: Platelet-derived Growth Factormentioning

confidence: 99%

“…In more detail, Fthenou et al have demonstrated significant co-stimulatory effects of chondroitin sulfate A and PDGF-BB in the modulation of the growth of HT1080 and B6FS fibrosarcoma cell lines (Fthenou et al, 2006). This co-stimulatory effect was perpetrated through more efficient signaling of tyrosine kinase receptors (Fthenou et al, 2006). On the other hand, it has been observed that HA suppresses PDGF beta-receptor activation, regulating in this manner the migration capacity of primary human dermal fibroblasts.…”

Section: Platelet-derived Growth Factormentioning

confidence: 99%

Hyaluronan/RHAMM Interactions in Mesenchymal Tumor Pathogenesis

Kouvidi

Nikitovic

Berdiaki

et al. 2014

Advances in Cancer Research

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Chondroitin sulfate A chains enhance platelet derived growth factor-mediated signalling in fibrosarcoma cells

Cited by 29 publications

References 36 publications

Increased expression of non-sulfated chondroitin correlates with adverse clinicopathological parameters in prostate cancer

Increased expression of non-sulfated chondroitin correlates with adverse clinicopathological parameters in prostate cancer

Sulfated sugars in the extracellular matrix orchestrate ovarian cancer development: ‘When sweet turns sour’

Hyaluronan/RHAMM Interactions in Mesenchymal Tumor Pathogenesis

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