Bi‐directional interactions of prostate cancer cells and bone marrow endothelial cells in three‐dimensional culture

Barrett, Jeffrey M.; Mangold, Kathy A.; Jilling, Tamás; Kaul, Karen L.

doi:10.1002/pros.20206

Cited by 28 publications

(22 citation statements)

References 17 publications

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“…The inhibitory effect of prostate cancer cells on LEC proliferation in vitro implies that cancer cells may also synthesize LEC mitogenesis inhibitors. Similarly, prostate cancer cells (PC-3, LNCaP, and DU145) have been shown to inhibit the in vitro growth of human bone marrow endothelial cells (37).…”

Section: Discussionmentioning

confidence: 99%

Tumor-Induced Activation of Lymphatic Endothelial Cells via Vascular Endothelial Growth Factor Receptor-2 Is Critical for Prostate Cancer Lymphatic Metastasis

et al. 2006

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Prostate cancer disseminates initially and primarily to regional lymph nodes. However, the nature of interactions between tumor cells and lymphatic endothelial cells (LEC) is poorly understood. In the current study, we have isolated prostate LECs and developed a series of two-dimensional and three-dimensional in vitro coculture systems and in vivo orthotopic prostate cancer models to investigate the interactions of prostate cancer cells with prostate LECs. In vitro, highly lymph node metastatic prostate cancer cell lines (PC-3 and LNCaP) and their conditioned medium enhanced prostate LEC tube formation and migration, whereas poorly lymph node metastatic prostate cancer cells (DU145) or normal prostate epithelial cells (RWPE-1) or their conditioned medium had no effect.

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Section: Discussionmentioning

confidence: 99%

Tumor-Induced Activation of Lymphatic Endothelial Cells via Vascular Endothelial Growth Factor Receptor-2 Is Critical for Prostate Cancer Lymphatic Metastasis

et al. 2006

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“…2). 23 HBME cells also stimulate proliferation of PC3 cells in coculture models 114. Therefore, bidirectional paracrine interactions between prostate cancer cells and HBME cells are likely important in metastatic spreading of prostate cancer to the bone 115…”

Section: Events In Prostate Cancer Metastatic Processmentioning

confidence: 99%

Steps in prostate cancer progression that lead to bone metastasis

Jin

Dayyani

Gallick

2011

Intl Journal of Cancer

160

149

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Prostate cancer is a complex disease in which metastasis to the bone is the main cause of death. Initial stages of metastasis are generally similar to those for most solid tumors; however, the mechanisms that underlie the homing of prostate tumor cells to the bone remain incompletely understood. Prostate cancer bone metastasis is also a microenvironment-driven disease, involving bi-directional interactions between the tumor and the bone microenvironment. In this review, we discuss the current understanding of the biologic processes and regulatory factors involved in the metastasis of prostate cancer cells, and their specific properties that promote growth in bone. Although many of these processes still need to be fully elucidated, a better understanding of the complex tumor/microenvironment interplay is slowly leading to more effective therapies for patients with prostate cancer bone metastases.

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“…Collagen gels were formed using eight parts acidified rat tail collagen (Roche Molecular Biochemical) reconstituted with one part 10ϫ concentrated DMEM and one part 10ϫ concentrated HBSS, and diluted to 1 mg/ml with DMEM containing 5% FBS and 50 ng/ml NGF, as previously described (Barrett et al, 2005). SMG were placed in collagenase solution for 20 min to enhance the permeability of the ganglion capsule, rinsed, and cut into four pieces under a dissecting microscope, then each piece was embedded into semisolidified collagen gels.…”

Section: Explant Culturesmentioning

confidence: 99%

Interleukin-17A Increases Neurite Outgrowth from Adult Postganglionic Sympathetic Neurons

Chisholm

Cervi²,

Nagpal³

et al. 2012

J. Neurosci.

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Bi‐directional interactions of prostate cancer cells and bone marrow endothelial cells in three‐dimensional culture

Abstract: Significant bi-directional interactions, including secreted factors and direct cellular interactions, exist between bone marrow endothelial cells and highly metastatic prostate cancer cells, and may underlie the propensity for prostate cancer to metastasize to the bone.

Cited by 28 publications

References 17 publications

Tumor-Induced Activation of Lymphatic Endothelial Cells via Vascular Endothelial Growth Factor Receptor-2 Is Critical for Prostate Cancer Lymphatic Metastasis

Tumor-Induced Activation of Lymphatic Endothelial Cells via Vascular Endothelial Growth Factor Receptor-2 Is Critical for Prostate Cancer Lymphatic Metastasis

Steps in prostate cancer progression that lead to bone metastasis

Interleukin-17A Increases Neurite Outgrowth from Adult Postganglionic Sympathetic Neurons

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