Influence of shear stress on tumor‐cell adhesion to endothelial‐cell extracellular matrix and its modulation by fibronectin

Bastida, E; Almirall, L; Bertomeu, Maria C.; Ordinas, Antonio

doi:10.1002/ijc.2910430635

Cited by 19 publications

(9 citation statements)

References 17 publications

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“…Although larger effects might seem more impressive, a moderate difference in adhesiveness may well have significant biological effects (and significant implications for a patient who may or may not progress to metastatic disease). Changes in cancer cell adhesion of this magnitude have previously been described and felt to be important in response to other stimuli by several other authors [Bastida et al, 1989;Haier and Nicolson, 2001;Mine et al, 2003]. Moreover, preexposing SW620 colon cells to such shear stress and turbulence not only increased adhesiveness but also increased Src kinase activity in a durable fashion.…”

Section: Discussionmentioning

confidence: 80%

“…Second, pretreatment of endothelial cells with IL-1 also increases Colo 201 colon cancer cell adhesion under low flow conditions [Yoshida et al, 1999]. Third, laminar flow promotes the adhesion of lung cancer cells [Bastida et al, 1989] and both promotes the adhesion of HT29 colon cancer cells and stabilizes already formed adhesions [Haier and Nicolson, 2000]. Indeed, one report suggests that Src may be involved in the effects of such laminar flow [Haier et al, 2002].…”

Section: Discussionmentioning

confidence: 93%

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Colon cancer cell adhesion in response to Src kinase activation and actin‐cytoskeleton by non‐laminar shear stress

Thamilselvan

Patel

Zyp

et al. 2004

J of Cellular Biochemistry

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Malignant cells shed from tumors during surgical resection or spontaneous metastasis experience physical forces such as shear stress and turbulence within the peritoneal cavity during irrigation, laparoscopic air insufflation, or surgical manipulation, and within the venous or lymphatic system. Since physical forces can activate intracellular signals that modulate the biology of various cell types in vitro, we hypothesized that shear stress and turbulence might increase colon cancer cell adhesion to extracellular matrix, potentiating metastatic implantation. Primary human malignant colon cancer cells isolated from resected tumors and SW620 were subjected to shear stress and turbulence by stirring cells in suspension at 600 rpm for 10 min. Shear stress for 10 min increased subsequent SW620 colon cancer cell adhesion by 40.0 +/- 3.0% (n = 3; P < 0.001) and primary cancer cells by 41.0 +/- 3.0% to collagen I when compared to control cells. In vitro kinase assay (1.5 +/- 0.13 fold) and Western analysis (1.34 +/- 0.04 fold) demonstrated a significant increase in Src kinase activity in cells exposed shear stress. Src kinase inhibitors PP1 (0.1 microM), PP2 (20 microM), and actin-cytoskeleton stabilizer phalloidin (10 microM) prevented the shear stress stimulated cell adhesion to collagen I. Furthermore, PP2 inhibited basal (50.0 +/- 2.8%) and prevented shear stress induced src activation but phalloidin pretreatment did not. These results raise the possibility that shear stress and turbulence may stimulate the adhesion of malignant cells shed from colon cancers by a mechanism that requires both actin-cytoskeletal reorganization an independent physical force activation of Src kinase. Blocking this pathway might reduce tumor metastasis during surgical resection.

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Section: Discussionmentioning

confidence: 80%

Section: Discussionmentioning

confidence: 93%

Colon cancer cell adhesion in response to Src kinase activation and actin‐cytoskeleton by non‐laminar shear stress

Thamilselvan

Patel

Zyp

et al. 2004

J of Cellular Biochemistry

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“…Some previous studies have discussed the influence of wall shear stress on cancer cell adhesion, and the tendencies were distinctly different in cell lines with differing metastatic properties (Haier and Nicolson 2001). For example, A-549 lung carcinoma cells (Bastida et al 1989) and MCF-7 human breast cancer cells (Moss et al 1999) were found to experience enhanced adhesion to the endothelium due to the added mechanical stimulus of shear stress. In the microchannel used in this study, the wall shear stress was higher on the inner wall than on the outer wall at the bifurcation and the confluence.…”

Section: Discussionmentioning

confidence: 95%

“…In former medical researches, adhesion phenomena on blood vessel walls have been investigated in great detail for leukocytes (e.g., Ostermann et al 2002;DiVietro et al 2007), malaria-infected RBCs (e.g., Scholander et al 1996;Beeson et al 2000) and cancer cells (e.g., Miles et al 2008;Glinskii et al 2005;Mine et al 2003;Fidler 2003;Chambers et al 2002). The effect of shear stress on the adhesion of cancer cells has also been thoroughly investigated (Bastida et al 1989;Moss et al 1999;Kitayama et al 2000;Thamilselvan et al 2004;Liang et al 2005Liang et al , 2008. Although these results provide evidence of the complex role of haemodynamic forces in the recruitment of metastatic cancer cells to endothelial cell, they do not provide enough information on how the channel geometry affects the adhesion phenomena.…”

Section: Introductionmentioning

confidence: 90%

Asymmetry of blood flow and cancer cell adhesion in a microchannel with symmetric bifurcation and confluence

Ishikawa

Fujiwara

Matsuki

et al. 2010

Biomed Microdevices

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Bifurcations and confluences are very common geometries in biomedical microdevices. Blood flow at microchannel bifurcations has different characteristics from that at confluences because of the multiphase properties of blood. Using a confocal micro-PIV system, we investigated the behaviour of red blood cells (RBCs) and cancer cells in microchannels with geometrically symmetric bifurcations and confluences. The behaviour of RBCs and cancer cells was strongly asymmetric at bifurcations and confluences whilst the trajectories of tracer particles in pure water were almost symmetric. The cell-free layer disappeared on the inner wall of the bifurcation but increased in size on the inner wall of the confluence. Cancer cells frequently adhered to the inner wall of the bifurcation but rarely to other locations. Because the wall surface coating and the wall shear stress were almost symmetric for the bifurcation and the confluence, the result indicates that not only chemical mediation and wall shear stress but also microscale haemodynamics play important roles in the adhesion of cancer cells to the microchannel walls. These results provide the fundamental basis for a better understanding of blood flow and cell adhesion in biomedical microdevices.

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“…Furthermore, biochemical interactions between adhesion molecules and their ligands during tumor cell adhesion within circulatory systems appear to be influenced by biophysical factors, such as shear stress caused by fluid flow, and cellular and soluble components of the circulating fluid. [15][16][17] Intravital microscopy technologies have been recently used to investigate metastatic tumor cell adhesion within host organ microcirculation, such as in liver and lung. 10 -14 In these studies contradictory results were reported regarding the type of entrapment (mechanical entrapment 10 -12 versus active cell adhesion 14,18 ) and the requirement of invasion into host organ parenchyma (invasion 10,11,13,18 versus intravascular proliferation 14 ).…”

mentioning

confidence: 99%

Organ-Specific Metastatic Tumor Cell Adhesion and Extravasation of Colon Carcinoma Cells with Different Metastatic Potential

Schlüter

Gaßmann

Enns

et al. 2006

The American Journal of Pathology

127

112

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Adhesive and invasive characteristics appear to be crucial for organ-specific metastasis formation. Using intravital microscopy we investigated the relation between the metastatic potential of colon carcinoma cells and their adhesive and invasive behavior during early steps of metastasis within microvasculatures of rat liver, lung, intestine, skin, muscle, spleen, and kidney in vivo. Colorectal carcinomas will affect ϳ6% of the population in the Western countries during their lifetime. These carcinomas are the third leading cause of cancer-related deaths among women and men and are the most important malignancies of the gut.1 Approximately 50% of the cancer patients die within 5 years because of cancerrelated problems, mostly attributable to metastatic lesions caused by the spread of cancers to near and distant sites. Even after potentially curative surgery, more than 30% of the patients with colorectal carcinomas subsequently develop metastases demonstrating that the spread from primary tumors to distant organs is usually the life-limiting aspect in colorectal carcinoma patients. 2Similar to other cancer entities, colorectal carcinomas often show organ preference of metastasis formation. The liver is the most common organ in which colorectal carcinomas establish distant metastases, and the liver is involved in more than 70% of patients with colorectal metastases. However, in 40 to 50% of these patients with liver metastases, other organs are also involved in metastatic colonization. The second most important organ for colorectal cancer metastasis is the lung, and 20 to 30% of all distant colorectal carcinoma metastases are found primarily in the lung. Isolated lung metastases with no evidence of other organ involvement are found in 5 to 10% of colorectal cancer patients. Other organs, such as the central nervous system, adrenal glands, spleen, skeleton, or skin together account for less than 10% of all colorectal metastases. 2,3The metastatic process consists of a number of sequential, interrelated steps that can all be rate limiting. 4,5 An important and early step during formation of distant metastasis appears to be the arrest of circulating tumor cells within the host organ.6,7 Approximately a century ago, two major hypotheses on the mechanisms of tumor cell arrest in metastatic host organs were proposed. Ewing 8 assumed that the random mechanical lodgment of Supported by the Innovative Medizinische Forschung Fund (University Hospital Mü nster) (Ha 1 2 01 01 to J.H.).K.S. and P.G. contributed equally to this study.

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Influence of shear stress on tumor‐cell adhesion to endothelial‐cell extracellular matrix and its modulation by fibronectin

Cited by 19 publications

References 17 publications

Colon cancer cell adhesion in response to Src kinase activation and actin‐cytoskeleton by non‐laminar shear stress

Colon cancer cell adhesion in response to Src kinase activation and actin‐cytoskeleton by non‐laminar shear stress

Asymmetry of blood flow and cancer cell adhesion in a microchannel with symmetric bifurcation and confluence

Organ-Specific Metastatic Tumor Cell Adhesion and Extravasation of Colon Carcinoma Cells with Different Metastatic Potential

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