Neutrophils influence melanoma adhesion and migration under flow conditions

Slattery, Margaret J.; Dong, Chuan

doi:10.1002/ijc.11297

Cited by 89 publications

(109 citation statements)

References 34 publications

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“…54 It has been shown in vitro that stationary neutrophils can facilitate tumor cell arrest and transmigration across endothelial monolayers via binding interactions between adherent neutrophils and passing tumor cells that are both adhesion molecule-and shear rate-dependent. 30,31,55,56 In vivo, we found that systemic inflammation increased tumor cell recruitment in the liver sinusoids when leukocytes simultaneously adhered in these vessels. Indeed, almost 80% of tumor cells were colocalized with adherent neutrophils in the sinusoids of LPS inflamed mice.…”

Section: Discussionmentioning

confidence: 83%

“…We asked whether sequestration of neutrophils, within the liver microvasculature contributed to the observed increase in tumor cell arrest in systemically inflamed animals, as has been suggested by the in vitro work of others. 30,31 First, the kinetics of LPS-induced leukocyte recruitment within the hepatic vasculature was measured by intravital microscopy as others and we previously described. 40,42,43 Leukocyte adhesion in sinusoids and postsinusoidal venules increased by 8-and 17.5-fold, respectively, relative to untreated controls (Figs.…”

Section: Leukocyte-tumor Cell Interactions Contribute To the Increasementioning

confidence: 99%

“…[27][28][29] Finally, there is emerging evidence, primarily based on in vitro studies, that a third cellular participant, the neutrophil, may contribute to inflammation-facilitated cancer cell adhesion. [30][31][32] Together, these findings suggest that states of systemic inflammation may favor the development of metastases by augmenting the recruitment of circulating tumor cells into organ tissues. However, the role of systemic inflammation in the metastatic spread of lung carcinoma has not been adequately studied in vivo.…”

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confidence: 99%

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Systemic inflammation increases cancer cell adhesion to hepatic sinusoids by neutrophil mediated mechanisms

McDonald

Spicer

Giannais

et al. 2009

Intl Journal of Cancer

204

163

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Interactions between endothelial selectins and selectin ligands expressed on tumor cells have been implicated in the binding of circulating metastatic cancer cells to the vascular endothelium during extravasation. Moreover, there is mounting evidence that inflammatory environments can accelerate the progression of metastasis by neutrophil mediated mechanisms. In this study, a physiologically relevant in vivo model of early metastasis coupled with intravital microscopy was used to visualize the trafficking of tumor cells within the liver vasculature in real time. Using GFPlabeled Lewis lung carcinoma subline H-59 cells, we show here that disrupting the interactions between endothelial selectins and tumor cell selectin ligands diminished tumor cell recruitment to the liver. Furthermore, systemic inflammation induced by intravenous injection of lipopolysaccharide significantly enhanced the metastatic potential of these lung carcinoma cells by increasing their propensity to adhere to the liver sinusoidal endothelium. Confocal microscopy revealed frequent colocalization of cancer cells with neutrophils and neutrophil depletion in vivo significantly attenuated the lipopolysaccharide-induced increase in H-59 cell adhesion. Although direct selectin-selectin ligand interactions contributed significantly to tumor cell adhesion to sinusoidal endothelial cells, we show here that in addition, interactions between adherent neutrophils within the inflamed sinusoids and circulating tumor cells may further increase tumor cell arrest in the liver. ' 2009 UICC Key words: cancer; metastasis; lung; rodent; adhesion molecules; e-selectin; neutrophil; sialyl Lewis X Lung cancer is the leading cause of cancer-related deaths worldwide. 1 A high proportion of patients harbor metastasis to regional lymph nodes upon presentation, and over half of all patients who undergo curative intent surgical resection of the lung will develop metastatic recurrence. 2 The liver is a common site of metastasis for lung cancer, with autopsy studies showing hepatic metastases in over 50% of lung cancer patients. 3 The hematogenous dissemination of cancer cells from a primary tumor to distant organs involves a cascade of sequential steps (reviewed in Refs. 4,5). The adhesion of circulating tumor cells to the vascular endothelium of distant organs is a key step in the metastatic cascade that may determine the organ tropism and extent of metastasis. Interactions between endothelial selectins and tumor cell selectin ligands have been implicated in the metastatic process. [5][6][7][8] Selectins are a family of transmembrane glycoproteins possessing an extracellular lectin domain that binds to carbohydrate moieties present on their ligands. 9 The three known selectins that function as cell adhesion molecules are expressed on the surface of endothelial cells (E-selectin and P-selectin), platelets (P-selectin) and leukocytes (L-selectin). E-selectin has been shown to contribute to the metastatic spread of multiple cancers, including lung and colon carcinoma, and m...

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Section: Discussionmentioning

confidence: 83%

Section: Leukocyte-tumor Cell Interactions Contribute To the Increasementioning

confidence: 99%

mentioning

confidence: 99%

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Systemic inflammation increases cancer cell adhesion to hepatic sinusoids by neutrophil mediated mechanisms

McDonald

Spicer

Giannais

et al. 2009

Intl Journal of Cancer

204

163

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“…In a mouse model, L-selectin on monocytes acting synergistically with P-selectin on platelets has been implicated in promoting colon cancer metastasis (14). It has also been shown that L-selectin expressed on human neutrophils is necessary to bind LS174T cells (15), but this molecule is apparently not involved in the neutrophil-mediated recruitment of melanoma cells (lacking L-selectin ligands) to stimulated endothelium (27).…”

Section: Discussionmentioning

confidence: 99%

HCELL Is the Major E- and L-selectin Ligand Expressed on LS174T Colon Carcinoma Cells

Burdick

Chu

Godar

et al. 2006

Journal of Biological Chemistry

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When confined to a primary site (early stage disease), the five-year survival rate from colon cancer is ϳ90%. However, when disseminated from primary sites (metastatic), survival drops precipitously to 8%. These dramatic survival statistics underscore the need to define the pathobiology of the metastatic process to devise novel interventions to prevent or inhibit colon cancer spread. Hematogenous metastasis occurs as a highly regulated cascade of events, initiated by the escape of tumor cells from the primary site into the blood stream and culminating in the formation of secondary colonies in distant organs. This process critically involves the binding of circulating colon cancer cells to the endothelium of target tissue(s) under fluid shear conditions, as well as the dynamic formation of leukocyte/cancer cell emboli, each of which are directed by selectin-selectin ligand interactions.The selectin family of adhesion molecules, E-, P-, and L-selectin, are Ca 2ϩ -dependent lectins that bind sialofucosylated carbohydrate structures, the prototypes of which are sialyl Lewis X (sLe x ) and sialyl Lewis A (sLe a ) (1, 2). E-and P-selectin are typically inducible endothelial molecules (P-selectin is also expressed on activated platelets), and L-selectin expression is restricted to leukocytes (3). There are multiple reports that tumor cell expression of E-selectin ligand(s) promotes the metastatic spread of numerous cancer types in vivo, including colon cancer (4 -10). Colon carcinoma cells also tether and roll under dynamic flow conditions on E-selectin purified and immobilized on plastic (11, 12), as well as E-selectin presented by cytokine-stimulated human umbilical vein endothelial cells (HUVEC) 2 (11-13). Independently, L-selectin has been shown to promote colon cancer metastasis in vivo (14), presumably mediated by the physical association of leukocytes with tumor cells resulting in leukocyte-colon cancer cell emboli (15, 16). Although expression of E-selectin ligand(s) on tumor cells itself promotes metastasis, one model holds that selectins work cooperatively to promote the spread of cancer; leukocyte L-selectin engagement of relevant tumor ligand(s) mediates the formation of leukocyte-tumor aggregates, which possess heightened binding capacity to endothelium in an E-selectindependent manner (16).Colon carcinoma cells express selectin ligands, and there is abundant evidence that selectin-dependent adhesive events are central to the metastatic process (4 -10,14). However, these selectin ligands have yet to be fully characterized or identified other than by general classifications (e.g. mucins). We recently identified the sialofucosylated hematopoietic cell E-and L-selectin ligand (HCELL) glycoform of CD44 on the LS174T colon carcinoma cell line and demonstrated its function as a high affinity E-and L-selectin ligand using the blot rolling assay (17, 18). However, these studies did not specifically address the relative contribution(s) of HCELL to the observed potent E-and L-selectin ligand activity of intact LS174...

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“…Neutrophils activated by melanoma-secreted IL-8 can facilitate melanoma cell extravasation through an interaction between ICAM-1 (CD54) on the melanoma cells and Mac-1 (CD11b/CD18) on neutrophils [253,254,293]. Neutrophils were also shown to be important for entrapping circulating melanoma cells and thus facilitating lung metastasis development [294].…”

Section: Promotion Of Cancer Cell Dissemination By Neutrophilsmentioning

confidence: 99%

The Multifaceted Roles Neutrophils Play in the Tumor Microenvironment

Sionov

Fridlender

Granot

2014

Cancer Microenvironment

342

261

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Neutrophils are myeloid cells that constitute 50-70 % of all white blood cells in the human circulation. Traditionally, neutrophils are viewed as the first line of defense against infections and as a major component of the inflammatory process. In addition, accumulating evidence suggest that neutrophils may also play a key role in multiple aspects of cancer biology. The possible involvement of neutrophils in cancer prevention and promotion was already suggested more than half a century ago, however, despite being the major component of the immune system, their contribution has often been overshadowed by other immune components such as lymphocytes and macrophages. Neutrophils seem to have conflicting functions in cancer and can be classified into anti-tumor (N1) and pro-tumor (N2) sub-populations. The aim of this review is to discuss the varying nature of neutrophil function in the cancer microenvironment with a specific emphasis on the mechanisms that regulate neutrophil mobilization, recruitment and activation.

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Neutrophils influence melanoma adhesion and migration under flow conditions

Cited by 89 publications

References 34 publications

Systemic inflammation increases cancer cell adhesion to hepatic sinusoids by neutrophil mediated mechanisms

Systemic inflammation increases cancer cell adhesion to hepatic sinusoids by neutrophil mediated mechanisms

HCELL Is the Major E- and L-selectin Ligand Expressed on LS174T Colon Carcinoma Cells

The Multifaceted Roles Neutrophils Play in the Tumor Microenvironment

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