The glycosaminoglycans of normal and hyperplastic prostate

Klerk, D.P. De

doi:10.1002/pros.2990040107

Cited by 34 publications

(27 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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“…In fact, HA overproduction is thought to be directly involved in prostate cancer progression. Histological sections of normal adult prostate tissue demonstrate the presence of HA in the prostate stroma (25,46). In cancerous human prostates, HA expression levels are increased on the carcinoma cells and correspond to dedifferentiation of the cancer (25,26).…”

Section: Discussionmentioning

confidence: 99%

“…Elevated levels of HA are associated with various pathologies, such as arthritis, inflammation, and several cancers (22)(23)(24), including prostate (25,26). Melanoma cells selected for high expression of HA were more metastatic when injected into nude mice than cells that expressed low amounts of HA (27).…”

mentioning

confidence: 99%

Hyaluronan Synthase Elevation in Metastatic Prostate Carcinoma Cells Correlates with Hyaluronan Surface Retention, a Prerequisite for Rapid Adhesion to Bone Marrow Endothelial Cells

Simpson¹,

Reiland²,

Burger³

et al. 2001

Journal of Biological Chemistry

100

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Bone marrow is the primary site of metastasis in patients with advanced stage prostate cancer. Prostate carcinoma cells metastasizing to bone must initially adhere to endothelial cells in the bone marrow sinusoids. In this report, we have modeled that interaction in vitro using two bone marrow endothelial cell (BMEC) lines and four prostate adenocarcinoma cell lines to investigate the adhesion mechanism. Highly metastatic PC3 and PC3M-LN4 cells were found to adhere rapidly and specifically (70 -90%) to BMEC-1 and trHBMEC bone marrow endothelial cells, but not to human umbilical vein endothelial cells (15-25%). Specific adhesion to BMEC-1 and trHBMEC was dependent upon the presence of a hyaluronan (HA) pericellular matrix assembled on the prostate carcinoma cells. DU145 and LNCaP cells were only weakly adherent and retained no cell surface HA. Maximal BMEC adhesion and HA encapsulation were associated with high levels of HA synthesis by the prostate carcinoma cells. Up-regulation of HA synthase isoforms Has2 and Has3 relative to levels expressed by normal prostate corresponded to elevated HA synthesis and avid BMEC adhesion. These results support a model in which tumor cells with up-regulated HA synthase expression assemble a cell surface hyaluronan matrix that promotes adhesion to bone marrow endothelial cells. This interaction could contribute to preferential bone metastasis by prostate carcinoma cells.

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“…Balancing family life and work was always a juggle but also very rewarding. (De Klerk 1983), my seminal studies demonstrated that the peritumoural stroma was the source of the increased CS (Ricciardelli et al 1997). Furthermore, I demonstrated that the level of CS in the peritumoural stroma was strongly associated with development of metastatic disease and an independent predictor of progression-free survival in a cohort of clinically localised prostate cancer (Ricciardelli et al 1997(Ricciardelli et al , 1999.…”

Section: :11mentioning

confidence: 99%

WOMEN IN CANCER PROFILE: My pathway to understanding the role of the tumour microenvironment in cancer progression

Ricciardelli

2016

Endocrine-Related Cancer

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The glycosaminoglycans of normal and hyperplastic prostate

Cited by 34 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

Hyaluronan Synthase Elevation in Metastatic Prostate Carcinoma Cells Correlates with Hyaluronan Surface Retention, a Prerequisite for Rapid Adhesion to Bone Marrow Endothelial Cells

WOMEN IN CANCER PROFILE: My pathway to understanding the role of the tumour microenvironment in cancer progression

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