Human endothelial precursor cells express tumor endothelial marker 1/endosialin/CD248

Bagley, Rebecca G.; Rouleau, Cecile; Martin, Thomas N.; Boutin, Paula; Weber, William; Ruzek, Melanie C.; Honma, Nakayuki; Nacht, Mariana; Shankara, Srinivas; Kataoka, Satoshi; Ishida, Isao; Roberts, Bruce; Teicher, Beverly A.

doi:10.1158/1535-7163.mct-08-0050

Cited by 51 publications

(36 citation statements)

References 38 publications

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“…The tubes/networks that MSC can establish may provide structural support in vivo as stroma or could potentially serve as a framework for vascular development during periods of active angiogenesis. Anti-endosialin was also effective at preventing tube/network formation by pericytes and endothelial precursor cells indicating that targeting endosialin can influence multiple cell types which contribute to tumor growth associated with vasculature and stroma (40,41).…”

Section: Discussionmentioning

confidence: 98%

Human mesenchymal stem cells from bone marrow express tumor endothelial and stromal markers

Weber¹,

Rouleau²,

Yang³

et al. 2009

Int J Oncol

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Abstract. Tumor development is a complex and dynamic process that involves malignant, vascular, and stromal cells. Endosialin is a tumor endothelial marker (TEM) present in the microvasculature and stroma of human tumors. Cancerassociated fibroblasts (CAF) have been implicated in promoting tumor development and have been associated with mesenchymal stem cells (MSC). Since stem/progenitor cells recruited either from bone marrow or residing in nearby tissues can contribute to pathological processes we investigated endosialin in MSC using a novel monoclonal antibody. Endosialin is highly expressed by CAF and human bone marrow-derived MSC. MSC can form networks in a tube formation assay that is inhibited by an anti-endosialin antibody. Immunohistochemistry for human endosialin in xenograft tumors following co-injection of MSC and cancer cells identified MSC in tumor stroma. MSC are a potential target for anticancer therapeutic intervention and endosialin expression offers a new tool for the identification of MSC. Endosialin expression by both CAF and MSC further implies the potential contribution of MSC to tumor stroma via differentiation into tumor stromal fibroblasts.

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Section: Discussionmentioning

confidence: 98%

Human mesenchymal stem cells from bone marrow express tumor endothelial and stromal markers

Weber¹,

Rouleau²,

Yang³

et al. 2009

Int J Oncol

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“…To this end, we examined the expression of endothelial precursor marker CD133, 30 CD248 (endosialin), 31 along with early and late mural cell markers calponin, desmin, and smooth muscle-␣ actin. Expression of CD133 and CD248 indicates that LEC/KSHV express endothelial precursor cell markers ( Figure 2A-B).…”

Section: Endothelial and Mural Cell Precursor Characteristics In Ks Cmentioning

confidence: 99%

KSHV-induced notch components render endothelial and mural cell characteristics and cell survival

Liu¹,

Li²,

Tulpule³

et al. 2010

Blood

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Kaposi sarcoma–associated herpesvirus (KSHV) infection is essential to the development of Kaposi sarcoma (KS). Notch signaling is also known to play a pivotal role in KS cell survival and lytic phase entrance of KSHV. In the current study, we sought to determine whether KSHV regulates Notch components. KSHV-infected lymphatic endothelial cells showed induction of receptors Notch3 and Notch4, Notch ligands Dll4 and Jagged1, and activated Notch receptors in contrast to uninfected lymphatic endothelial cells. In addition, KSHV induced the expression of endothelial precursor cell marker (CD133) and mural cell markers (calponin, desmin, and smooth muscle alpha actin), suggesting dedifferentiation and trans-differentiation. Overexpression of latency proteins (LANA, vFLIP) and lytic phase proteins (RTA, vGPCR, viral interleukin-6) further supported the direct regulatory capacity of KSHV viral proteins to induce Notch receptors (Notch2, Notch3), ligands (Dll1, Dll4, Jagged1), downstream targets (Hey, Hes), and endothelial precursor CD133. Targeting Notch pathway with γ-secretase inhibitor and a decoy protein in the form of soluble Dll4 inhibited growth of KSHV-transformed endothelial cell line. Soluble Dll4 was also highly active in vivo against KS tumor xenograft. It inhibited tumor cell growth, induced tumor cell death, and reduced vessel perfusion. Soluble Dll4 is thus a candidate for clinical investigation.

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“…15 Subsequently, TEM-1/collagen IV co-localization was confirmed by confocal microscopy. 10 Other studies have demonstrated the importance of TEM-1 in regulating proliferation, 12 tube formation on matrigel, 11,16 and cell migration. 11,12 However, the exact mechanism(s)…”

Section: Introductionmentioning

confidence: 99%

Endosialin/TEM-1/CD248 regulates pericyte proliferation through PDGF receptor signaling

Tomkowicz

Rybiński²,

Sebeck³

et al. 2010

Cancer Biology & Therapy

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Human endothelial precursor cells express tumor endothelial marker 1/endosialin/CD248

Abstract: Angiogenesis occurs during normal physiologic processes as well as under pathologic conditions such as tumor growth.

Cited by 51 publications

References 38 publications

Human mesenchymal stem cells from bone marrow express tumor endothelial and stromal markers

Human mesenchymal stem cells from bone marrow express tumor endothelial and stromal markers

KSHV-induced notch components render endothelial and mural cell characteristics and cell survival

Endosialin/TEM-1/CD248 regulates pericyte proliferation through PDGF receptor signaling

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