Effects of the Tumor-Leukocyte Microenvironment on Melanoma–Neutrophil Adhesion to the Endothelium in a Shear Flow

Liang, Shuang; Hoskins, Meghan H.; Khanna, Payal; Kunz, Robert F.; Dong, Chuan

doi:10.1007/s12195-008-0016-8

Cited by 26 publications

(27 citation statements)

References 28 publications

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“…27 Tumor cells have been reported to undergo extensive interactions with host cells including polymorphonuclear cells (PMNs). 98 Such interactions between cancer cells and PMNs together with the normal interactions between PMNs and endothelial cells have been observed in breast cancer, advanced gastric cancer, colon cancer, and malignant melanoma, 95,128,173 and could play important roles in cancer cell transendothelial migration under physiological flow conditions, 97,144 although the mechanism remains unclear. To address this, Liang et al 97 examined the molecular interactions between endothelial cells, PMNs, and melanoma cells under defined hydrodynamic shear conditions and found that PMN-facilitated melanoma adhesion to endothelial cells is shear dependent.…”

Section: Metastatic Cascade: Adhesive Recruitment Of Cancer Cells Viamentioning

confidence: 99%

Glycomechanics of the Metastatic Cascade: Tumor Cell–Endothelial Cell Interactions in the Circulation

2011

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Hydrodynamic shear force plays an important role in the leukocyte adhesion cascade that involves the tethering and rolling of cells along the endothelial layer, their firm adhesion or arrest, and their extravasation or escape from the circulatory system by inducing passive deformation, or cell flattening, and microvilli stretching, as well as regulating the expression, distribution, and conformation of adhesion molecules on leukocytes and the endothelial layer. Similarly, the dissemination of circulating tumor cells (CTCs) from the primary tumor sites is believed to involve tethering, rolling, and firm adhesion steps before their eventual extravasation which leads to secondary tumor sites (metastasis). Of particular importance to both the leukocyte adhesion cascade and the extravasation of CTCs, glycoproteins are involved in all three steps (capture, rolling, and firm adhesion) and consist of a variety of important selectin ligands. This review article provides an overview of glycoprotein glycosylation associated with the abnormal glycan expression on cancer cell surfaces, where well-established and novel selectin ligands that are cancer related are discussed. An overview of computational approaches on the effects of fluid mechanical force on glycoprotein mediated cancer cell rolling and adhesion is presented with a highlight of recent flow-based and selectin-mediated cell capturing/enriching devices. Finally, as an important branch of the glycoprotein family, mucins, specifically MUC1, are discussed in the context of their aberrant expression on cancer cells and their role as cancer cell adhesion molecules. Since metastasis relies heavily on glycoprotein interactions in the bloodstream where the fluid shear stress highly regulates cell adhesion forces, it is important to study and understand the glycomechanics of all relevant glycoproteins (well-established and novel) as they relate to the metastatic cascade.

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Section: Metastatic Cascade: Adhesive Recruitment Of Cancer Cells Viamentioning

confidence: 99%

Glycomechanics of the Metastatic Cascade: Tumor Cell–Endothelial Cell Interactions in the Circulation

2011

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“…In gastric adenocarcinomas, the release of mast cell mediators is associated with changes in the microvascular basal lamina that mediate the blood vessel remodeling [9,10]. In addition, Liang et al [11] observed that the interaction between neutrophils and melanoma cells through adhesion molecules facilitates tumor cell migration into the vascular endothelium and metastasis. Further, under conditions in which the chronic inflammatory status of the solid tumor becomes acute, neutrophils can be converted into antitumor effector cells, as demonstrated in rodent studies and clinical trials of long-term granulocyte colony-stimulating factor use [12].…”

Section: Introductionmentioning

confidence: 99%

Myenteric Denervation Downregulates Galectin-1 and -3 Expression in Gastric Carcinogenesis

Estofolete

Zucoloto²,

Oliani

et al. 2010

Dig Dis Sci

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“…ing CTCs to end-organ endothelium, have been described (19). This interaction is mediated by the interaction of β 2 integrins on neutrophils and ICAM-1 on tumor cells (31,(35)(36)(37). Additional contact-independent mechanisms have also been proposed.…”

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confidence: 99%

Neutrophil extracellular traps sequester circulating tumor cells and promote metastasis

Cools-Lartigue¹,

Spicer²,

McDonald³

et al. 2013

J. Clin. Invest.

1,118

1,025

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The majority of patients with cancer undergo at least one surgical procedure as part of their treatment. Severe postsurgical infection is associated with adverse oncologic outcomes; however, the mechanisms underlying this phenomenon are unclear. Emerging evidence suggests that neutrophils, which function as the first line of defense during infections, facilitate cancer progression. Neutrophil extracellular traps (NETs) are extracellular neutrophil-derived DNA webs released in response to inflammatory cues that trap and kill invading pathogens. The role of NETs in cancer progression is entirely unknown. We report that circulating tumor cells become trapped within NETs in vitro under static and dynamic conditions. In a murine model of infection using cecal ligation and puncture, we demonstrated microvascular NET deposition and consequent trapping of circulating lung carcinoma cells within DNA webs. NET trapping was associated with increased formation of hepatic micrometastases at 48 hours and gross metastatic disease burden at 2 weeks following tumor cell injection. These effects were abrogated by NET inhibition with DNAse or a neutrophil elastase inhibitor. These findings implicate NETs in the process of cancer metastasis in the context of systemic infection and identify NETs as potential therapeutic targets. IntroductionCancer remains a devastating cause of mortality worldwide, with the majority of patients dying as a result of metastasis (1-3). Currently, locoregional control in the form of complete oncologic resection remains an essential curative modality for nearly all solid tumors and provides improved overall and disease-free survival (2, 4,5). Control of distant recurrence is predominantly achieved through systemic chemotherapy, with variable results (6-8). However, standard oncologic interventions can have negative consequences. First, manipulation of the primary tumor during surgery is associated with increased numbers of circulating tumor cells (CTCs) (9). Second, infectious complications occur as a result of cancer progression itself, such as bowel obstruction or pneumonia (10, 11), and due to complications of standard cancer treatments, such as chemotherapy and surgery (12)(13)(14).Postsurgical infections occur with alarming frequency, with an incidence approaching 40% in some series (15)(16)(17). Given that the majority of the nearly 2 million patients diagnosed with cancer in 2012 in the United States alone underwent at least one surgical procedure, the tremendous potential burden of infection becomes apparent (18). One disturbing feature of severe infectious complications in patients with cancer is their association with adverse oncologic outcomes independent of the morbidity associated with the infectious insult (14,(19)(20)(21). This phenomenon has been observed across a broad range of malignancies, including lung, esophageal, breast, ovarian, and colorectal cancer, whereby severe postoperative infectious complications, such as pneumonia, peritonitis, and sepsis, are significantly associated wit...

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Effects of the Tumor-Leukocyte Microenvironment on Melanoma–Neutrophil Adhesion to the Endothelium in a Shear Flow

Cited by 26 publications

References 28 publications

Glycomechanics of the Metastatic Cascade: Tumor Cell–Endothelial Cell Interactions in the Circulation

Glycomechanics of the Metastatic Cascade: Tumor Cell–Endothelial Cell Interactions in the Circulation

Myenteric Denervation Downregulates Galectin-1 and -3 Expression in Gastric Carcinogenesis

Neutrophil extracellular traps sequester circulating tumor cells and promote metastasis

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