Tumor cell adhesion under hydrodynamic conditions of fluid flow

Haier, Jörg; Nicolson, Garth L.

doi:10.1034/j.1600-0463.2001.d01-118.x

Cited by 71 publications

(65 citation statements)

References 127 publications

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“…The adhesive ability of tumor cells to substrata plays a critical role for a successful metastasis (Haier and Nicolson, 2001). In this study, we investigate a molecular mechanism of the inside-out signaling that regulates the adhesive ability of AR-positive PCa cells utilizing non-coated substrata.…”

Section: Discussionmentioning

confidence: 99%

ErbB-2 via PYK2 upregulates the adhesive ability of androgen receptor-positive human prostate cancer cells

et al. 2007

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Aberrant regulation in the adhesive ability of cancer cells is closely associated with their metastatic activity. In this study, we examine the role of ErbB-2 in regulating the adhesive ability of androgen receptor (AR)-positive human prostate cancer (PCa) cells, the major cell population of PCa. Utilizing different LNCaP and MDA PCa2b cells as model systems, we found that ErbB-2 activity was correlated with PYK2 activity and adhesive ability in those cells. Increased ErbB-2 expression or activity in LNCaP C-33 cells enhanced PYK2 activation and cell adhesion, while the high PYK2 activity and the rapid adhesion of LNCaP C-81 cells were decreased by diminishing ErbB-2 expression or activity. Knockdown studies revealed the predominant role of ErbB-2 in regulating LNCaP C-81 cell adhesion. Coimmunoprecipitation showed that C-81 cells had increased interaction between ErbB-2 and PYK2. Elevated ErbB-2 activity in LNCaP cells correlated with increased ERK/MAPK activity and enhanced adhesive ability, which were abolished by the expression of K457A-PYK2 mutant or the treatment of PD98059, a MEK inhibitor. In summary, our data suggested that ErbB-2, via PYK2-ERK/MAPK, upregulates the adhesive ability of AR-positive human PCa cells.

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Section: Discussionmentioning

confidence: 99%

ErbB-2 via PYK2 upregulates the adhesive ability of androgen receptor-positive human prostate cancer cells

et al. 2007

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“…In fact, it will be interesting to test whether the selection of galectin-7 that we have observed in aggressive lymphoma cells, such as in S19 and K3.1, can also occur in ICAM-1-deficient mice, as adhesion molecules expressed on EC play a critical role in inducing bidirectional signalling that leads to the expression of genes that confer tumor cells with an aggressive behavior. 44,45 The role of galectin-7 in cancer has previously been implied in a rat model of chemically induced mammary carcinoma. 22 Galectin-7 was originally identified in the human epidermis and later found to be expressed in all types of stratified epithelial cells in the skin, tongue, esophagus, and Hassal's corpuscles in the thymus.…”

Section: Figurementioning

confidence: 99%

Upregulation of galectin-7 in murine lymphoma cells is associated with progression toward an aggressive phenotype

et al. 2003

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We have previously shown that ICAM-1-deficient mice were resistant to lymphoma dissemination of intravenously injected 164T2 lymphoma cells. Highly aggressive variants of this cell line, however, could overcome this resistance. To discern the complex pattern of gene expression involved in the evolution of aggressiveness in lymphoma cells, we compared the transcriptome of 164T2 cells with that of their aggressive variants using cDNA arrays. We identified several genes that were differentially expressed in nonmetastatic lymphoma cells and their metastatic variants. Galectin-7, associated with the development of chemically induced mammary carcinoma, was one such gene whose expression was significantly upregulated. We showed that it was constitutively expressed in aggressive variants, at both mRNA and protein levels. Galectin-7 expression in aggressive lymphoma cells was induced upon in vivo selection in several organs, including the thymus, the spleen and kidneys. We also showed that treatment of nonaggressive lymphoma cells with 5-aza-2 0 -deoxycytidine was sufficient to induce galectin-7 gene expression. This report is the first to show that galectin-7 is expressed in aggressive lymphoma.

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“…Tumor cell metastasis is a highly regulated and dynamic process in which cancer cells separate from a primary tumor, migrate across blood vessel walls into the bloodstream, and disperse throughout the body to generate colonies [1]. Hematogenous tumor cell dissemination depends on cell adhesive interactions that are mediated by adhesion receptors, such as selectins and integrins [2][3][4][5].…”

Section: Introductionmentioning

confidence: 99%

P-selectin activates integrin-mediated colon carcinoma cell adhesion to fibronectin

Reyes‐Reyes

George

Roberts

et al. 2006

Experimental Cell Research

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During hematogenous cancer metastasis, tumor cells separate from a primary mass, enter the bloodstream, disperse throughout the body, migrate across vessel walls, and generate distant colonies. The later steps of metastasis superficially resemble leukocyte extravasation, a process initiated by selectin-mediated cell tethering to the blood vessel wall followed by integrin-mediated arrest and transendothelial migration. Some cancer cells express P-selectin ligands and attach to immobilized Pselectin, suggesting that these cells can arrest in blood vessels using sequential selectin-and integrin-mediated adhesion, as do leukocytes. We hypothesize that selectin binding may regulate subsequent integrin-mediated steps in metastasis. Using a model system of cultured Colo 320 human colon adenocarcinoma cells incubated with soluble P-selectin-IgG chimeric protein, we have found that P-selectin can stimulate activation of the α 5 β 1 integrin resulting in a specific increase of adhesion and spreading of these cells on fibronectin substrates. P-selectin binding also induced activation of p38 mitogen-activated protein kinase (p38 MAPK) and phosphatidylinositol 3-kinase (PI3-K). PI3-K inhibitors blocked P-selectin-mediated integrin activation, cell attachment, and cell spreading. Inhibition of p38 MAPK activation blocked cell spreading, but not cell attachment. P-Selectin binding also resulted in formation of a signaling complex containing PI3-K and p38 MAPK. These results suggest that P-selectin binding to tumor cells can activate α 5 β 1 integrin via PI3-K and p38 MAPK signaling pathways leading to increased cell adhesion. We propose that P-selectin ligands are important tumor cell signaling molecules that modulate integrin-mediated cell adhesion in the metastatic process.

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Tumor cell adhesion under hydrodynamic conditions of fluid flow

Cited by 71 publications

References 127 publications

ErbB-2 via PYK2 upregulates the adhesive ability of androgen receptor-positive human prostate cancer cells

ErbB-2 via PYK2 upregulates the adhesive ability of androgen receptor-positive human prostate cancer cells

Upregulation of galectin-7 in murine lymphoma cells is associated with progression toward an aggressive phenotype

P-selectin activates integrin-mediated colon carcinoma cell adhesion to fibronectin

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