Glycosaminoglycans of Human Prostatic Cancer

Klerk, D.P. De; Lee, D.V.; Human, H.J.

doi:10.1016/s0022-5347(17)50750-8

Cited by 45 publications

(37 citation statements)

References 24 publications

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“…Histopathologic studies of human prostate cancer have shown that HA levels increase in tumors as a function of increasing pathologic grade (13,14). These data suggest that tumor cells may develop an enhanced capacity to synthesize and retain pericellular HA.…”

Section: Discussionmentioning

confidence: 96%

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Manipulation of Hyaluronan Synthase Expression in Prostate Adenocarcinoma Cells Alters Pericellular Matrix Retention and Adhesion to Bone Marrow Endothelial Cells

Simpson¹,

Wilson²,

Furcht³

et al. 2002

Journal of Biological Chemistry

104

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Prostate cancer metastasis to bone marrow involves initial adhesion of tumor cells to the bone marrow endothelium, followed by transmigration and proliferation within the marrow. Rapid, specific adhesion of highly metastatic prostate adenocarcinoma cells Prostate cancer mortality is frequently the result of bone metastasis. The preferential homing of circulating prostate tumor cells to bone marrow is thought to involve an initial rapid adhesion to cells of the bone marrow endothelium, followed by transmigration of the endothelium, engagement of specific receptors, and subsequent proliferation within the bone marrow microenvironment. Molecular mechanisms underlying these processes are poorly understood, but there is evidence that tumor cells may exploit existing pathways utilized by circulating blood cell progenitors to gain access to bone marrow.To identify potential cell adhesion molecules involved in prostate tumor bone metastasis, research in our laboratory has focused on the interaction of prostate carcinoma cells with bone marrow endothelial cells (BMECs).1 Highly metastatic PC3M-LN4 cells (1) were found to adhere rapidly to human bone marrow-derived sinusoidal endothelial cell lines, whereas poorly metastatic LNCaP cells were only weakly adherent (2). This adhesion, specific for BMECs relative to other endothelial cells, was subsequently found to depend upon the presence of a pericellular hyaluronan (HA) matrix assembled on the PC3M-LN4 cells. The presence of pericellular HA further correlated with elevated HA synthesis and expression of HA biosynthetic enzymes in the metastatic cells. Collectively, our results may implicate tumor cell-associated HA and up-regulation of HA synthase (HAS) in prostate cancer progression, possibly by facilitating arrest in the bone microvasculature and/or preferential tissue colonization of individual tumor cells.

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Section: Discussionmentioning

confidence: 96%

“…Production of HA is thought to be directly involved in prostate cancer progression. In human cancerous prostates, HA levels are increased on the carcinoma cells and correspond to dedifferentiation of the cancer (13,14).…”

mentioning

confidence: 99%

Manipulation of Hyaluronan Synthase Expression in Prostate Adenocarcinoma Cells Alters Pericellular Matrix Retention and Adhesion to Bone Marrow Endothelial Cells

Simpson¹,

Wilson²,

Furcht³

et al. 2002

Journal of Biological Chemistry

104

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show abstract

“…Instead, a decrease in the expression of cell surface HSPGs, the amount of heparan sulfate, the fraction of total glycosaminoglycan present as heparan sulfate, and the extent of sulfation of heparan sulfate, has been reported in association with cancers of the bladder, prostate, and lung (59)(60)(61)(62) and with the oncogenic activation of cells in vitro (63). Furthermore, in squamous cell carcinomas, the level of syndecan-1 correlates inversely with tumor grade, stage and clinical outcome (64).…”

Section: Discussionmentioning

confidence: 99%

The cell-surface heparan sulfate proteoglycan glypican-1 regulates growth factor action in pancreatic carcinoma cells and is overexpressed in human pancreatic cancer.

et al. 1998

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“…The concentration of chondroitin sulfate is greatly increased over normal tissue levels in several different malignancies (7)(8)(9)(10), including prostate cancer (11)(12)(13). Our previous studies illustrated that patients treated by radical prostatectomy for early stage (cT 1 -cT 2 ) cancer who showed high chondroitin sulfate concentration in the peritumoral stroma of the prostate had a significantly higher incidence of PSA failure than patients with low chondroitin sulfate concentration (14).…”

Section: Introductionmentioning

confidence: 99%

Immunohistochemical Level of Unsulfated Chondroitin Disaccharides in the Cancer Stroma Is an Independent Predictor of Prostate Cancer Relapse

Sakko

Butler

Byers

et al. 2008

Cancer Epidemiology, Biomarkers &Amp; Prevention

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The glycosaminoglycan chondroitin sulfate is significantly increased in the peritumoral stroma of prostate tumors compared with normal stroma and is an independent predictor of prostate-specific antigen (PSA) relapse following radical prostatectomy. In this study, we determined whether specific alterations in the sulfation pattern of glycosaminoglycan chains in clinically organ-confined prostate cancer are associated with PSA relapse. Immunoreactivity to distinct glycosaminoglycan disaccharide epitopes was assessed by manually scoring the staining intensity in prostate tissues from patients with benign prostatic hyperplasia (n = 19), early-stage cancer (cohort 1, n = 55 and cohort 2, n = 275), and advanced-stage cancer (n = 20). Alterations to glycosaminoglycans in benign and malignant prostate tissues were determined by cellulose acetate chromatography and high-pressure liquid chromatography. Glycosaminoglycan disaccharide epitopes were localized to the peritumoral stroma of clinically localized prostate cancer. The level of immunostaining for unsulfated disaccharides (C0S) in the peritumoral stroma, but not for 4-sulfated (C4S) or 6-sulfated disaccharides (C6S), was significantly associated with the rate of PSA relapse following radical prostatectomy. High levels of C0S immunostaining were determined to be an independent predictor of PSA relapse (1.6-fold, P = 0.020). Advanced-stage prostate cancer tissues exhibited reduced electrophoretic mobility for chondroitin sulfate and increased unsulfated disaccharides when compared with benign prostatic hyperplasia tissues, whereas the sulfated disaccharide levels were unaffected. The level of C0S immunostaining in the peritumoral stroma is an independent determinant of PSA failure in clinically localized prostate cancer. Specific alterations to chondroitin sulfate side chains occurring during tumor development may be a crucial step for disease progression in prostate cancer. (Cancer Epidemiol Biomarkers Prev 2008;17(9):2488 -97)

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Glycosaminoglycans of Human Prostatic Cancer

Cited by 45 publications

References 24 publications

Manipulation of Hyaluronan Synthase Expression in Prostate Adenocarcinoma Cells Alters Pericellular Matrix Retention and Adhesion to Bone Marrow Endothelial Cells

Manipulation of Hyaluronan Synthase Expression in Prostate Adenocarcinoma Cells Alters Pericellular Matrix Retention and Adhesion to Bone Marrow Endothelial Cells

The cell-surface heparan sulfate proteoglycan glypican-1 regulates growth factor action in pancreatic carcinoma cells and is overexpressed in human pancreatic cancer.

Immunohistochemical Level of Unsulfated Chondroitin Disaccharides in the Cancer Stroma Is an Independent Predictor of Prostate Cancer Relapse

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