Tumor cell adhesion of human colon carcinoma cells with different metastatic properties to extracellular matrix under dynamic conditions of laminar flow

Haier, Jörg; Nicolson, Garth L.

doi:10.1007/s004320000161

Cited by 21 publications

(19 citation statements)

References 24 publications

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“…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: 96%

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: 96%

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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“…Adhesion molecules, including integrins and selectins, are known to play important roles in the interaction of cancer cells with the vessel walls in the target organ [7,8]. Basement membrane [9,10] proteins and integrins [11] can profoundly affect the biological behaviour of metastatic tumour cells. For example, collagen type-IV inhibits melanoma cell proliferation and promotes its adhesion [12].…”

Section: Introductionmentioning

confidence: 99%

Collagen type IV, laminin, α-smooth muscle actin (αSMA), α1 and α6 integrins expression in the liver with metastases from malignant gastrointestinal tumours

Gulubova

2004

Clin Exp Metastasis

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Basement membrane proteins and integrins can profoundly affect the biological behaviour of metastasic tumour cells. Using light and ultrastructural immunohistochemistry, we showed the presence of alterations in the occurrence of collagen type IV and laminin, and the expression of alpha1 and alpha6 integrin chains in the livers of patients with metastases from gastric, colorectal and pancreatic cancers. The myofibroblast-like cells in the metastatic stroma were studied. Parallel expressions of alpha-SMA, collagen type IV and alpha1 integrin chain, and appearance of laminin and alpha6 integrin chain immunoreactivity in the extratumoral liver tissue were markedly increased in sinusoids associated with metastases. Furthermore, ultrastructural immunohistochemistry detected tumour cells adhered to amorphous laminin deposits in the metastases. Laminin occurrence in liver sinusoids was visible as fine amorphous deposits in the space of Disse. The similarity between alpha-SMA-positive stromal cells in metastatic stroma and hepatic stellate cells (HSCs) was established by the presence of lipid droplets in their cytoplasm. The immune deposits of alpha1 and alpha6 integrin chains were observed on the hepatocyte microvilli and on the membrane of sinusoidal endothelial cells. These findings suggest that metastatic cells produce stimuli that induce HSCs activation and sinusoidal changes. In addition, the enhanced parallel expression of alphaSMA, collagen type IV, laminin and of alpha1 and alpha6 integrin chains in sinusoids associated with metastases, might potentiate the further dissemination of tumour cells in new liver areas.

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“…Studies from our laboratories (11, 12) as well as other investigators (13) have recently shown that another lectin, galectin-3, plays a key role in initiating the adhesion of human breast and prostate cancer cells to the endothelium by specifically interacting with the cancerassociated carbohydrate, T antigen. However, these studies were carried out under static conditions, and the relevance of galectin-3-T antigen interactions in mediating cancer cell adhesion under conditions of flow has not been investigated.Shear forces have an important influence on cell adhesion and other cellular functions, and malignant cell lines appear to possess different adhesive properties under static and dynamic conditions (14,15). To elucidate the molecular mechanisms of intercellular adhesive interactions relevant to breast cancer metastasis, we examined the adhesive behavior of two human breast carcinoma cell lines exhibiting distinct metastatic po-…”

mentioning

confidence: 99%

“…Shear forces have an important influence on cell adhesion and other cellular functions, and malignant cell lines appear to possess different adhesive properties under static and dynamic conditions (14,15). To elucidate the molecular mechanisms of intercellular adhesive interactions relevant to breast cancer metastasis, we examined the adhesive behavior of two human breast carcinoma cell lines exhibiting distinct metastatic po-…”

mentioning

confidence: 99%

MDA-MB-435 Human Breast Carcinoma Cell Homo- and Heterotypic Adhesion under Flow Conditions Is Mediated in Part by Thomsen-Friedenreich Antigen-Galectin-3 Interactions

Khaldoyanidi¹,

Glinsky²,

Sikora³

et al. 2003

Journal of Biological Chemistry

197

162

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Understanding cellular and molecular mechanisms of tumor metastasis is critically important for the development of new approaches to cancer treatment. One of the rate-limiting steps in metastatic dissemination is the adhesion of circulating cancer cells to the microvascular endothelium (for review, see Ref. 1). Recent experimental evidence identified endotheliumattached blood-born tumor cells as the seeds of secondary tumors (2). In the lung, early metastatic colonies were entirely within the blood vessels, and hematogenous metastases originated from the intravascular proliferation of tumor cells anchored to the endothelia (2). These results underscored the significance of intravascular intercellular adhesion in cancer metastasis.Although there is a substantial body of evidence demonstrating the role of various adhesion molecules in tumor cell adhesion (1, 3), the molecular and cellular mechanisms of cancer cell adhesion are still often modeled after the dynamics of the leukocyte adhesion cascade. Despite the many physical similarities, interaction of leukocytes and circulating malignant cells with the vascular endothelium are likely to be driven by distinct molecular mechanisms. For example, it is well documented that under conditions of shear force, circulating leukocytes participate in a multi-step cascade of sequential adhesion events involving rolling, adhesion, and transmigration across the vascular wall, where rolling is the first and rate-limiting step ultimately required for stable leukocyte adhesion to the endothelial cells (EC) 1 (4). However, in contrast to leukocytes, published data regarding the rolling and adhesion of tumor cells on vascular endothelium suggest a non-leukocyte-like mechanism (5-9). Furthermore, it is also not clear whether this step is required for stable adhesion of tumor cells to the endothelium. Leukocyte rolling is mostly mediated by the interaction of the members of C-type lectin family, selectins, with their cognate carbohydrate ligands (4, 10). Studies from our laboratories (11, 12) as well as other investigators (13) have recently shown that another lectin, galectin-3, plays a key role in initiating the adhesion of human breast and prostate cancer cells to the endothelium by specifically interacting with the cancerassociated carbohydrate, T antigen. However, these studies were carried out under static conditions, and the relevance of galectin-3-T antigen interactions in mediating cancer cell adhesion under conditions of flow has not been investigated.Shear forces have an important influence on cell adhesion and other cellular functions, and malignant cell lines appear to possess different adhesive properties under static and dynamic conditions (14,15). To elucidate the molecular mechanisms of intercellular adhesive interactions relevant to breast cancer metastasis, we examined the adhesive behavior of two human breast carcinoma cell lines exhibiting distinct metastatic po-

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Tumor cell adhesion of human colon carcinoma cells with different metastatic properties to extracellular matrix under dynamic conditions of laminar flow

Cited by 21 publications

References 24 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

Collagen type IV, laminin, α-smooth muscle actin (αSMA), α1 and α6 integrins expression in the liver with metastases from malignant gastrointestinal tumours

MDA-MB-435 Human Breast Carcinoma Cell Homo- and Heterotypic Adhesion under Flow Conditions Is Mediated in Part by Thomsen-Friedenreich Antigen-Galectin-3 Interactions

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