Stimulation of be-ta1 integrin down-regulates ICAM-1 expression and ICAM-1 dependent adhesion of lung cancer cells through focal adhesion kinase

Yasuda, Manabu; Tanaka, Yoshiya; Sugaya, Masakazu; So, Tetsuya; Eifuku, Ryozo; Imahayashi, Satoru; Yoshimatsu, Takashi; Oyama, Tsunehiro; Eto, Sumiya; Yasumoto, Kosei

doi:10.1016/s0169-5002(00)80670-4

Cited by 21 publications

(21 citation statements)

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“…Integrins, in turn, have been reported to downregulate ICAM1 expression via FAK [63] , suggesting that migration requires the downregulation of this adhesion molecule. It was therefore not surprising at first that FGF2 decreased ICAM1 expression while increasing migration via CCL2, all phenomena depending on FAK.…”

Section: Discussionmentioning

confidence: 99%

JNK/ERK/FAK Mediate Promigratory Actions of Basic Fibroblast Growth Factor in Astrocytes via CCL2 and COX2

Lichtenstein¹,

Madrigal

Pujol³

et al. 2012

Neurosignals

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While the role of cytokines in causing pro- and anti-inflammatory cascades in the brain and that of chemokines in promoting chemotaxis is well recognized, the immunomodulatory actions of neurotrophins released during brain injury remains largely undetermined. This knowledge gap affects basic fibroblast growth factor (FGF2), which in the brain is mainly produced by astrocytes and characteristically upregulated in reactive astrocytes. The goal of this study was to characterize the inflammatory actions of FGF2 in astrocytes using primary cultures. We report that FGF2 induced the upregulation of monocyte chemoattractant protein (CCL2) and cyclo-oxygenase type 2 (COX2), and the inhibition of lipopolysaccharide-elicited ICAM1 upregulation. The effects of FGF2 were: (i) dependent on gene transcription as revealed by the concomitant regulation of CCL2 or ICAM1 mRNAs; (ii) mediated by the FGF2 receptor type 2; (iii) dependent on ERK, JNK and FAK, and (iv) NF-ĸB-independent. FGF2 also caused accelerated wound closure dependent on CCL2, COX2, ERK, JNK and FAK in a scratch assay. We conclude that the signaling network triggered by FGF2 in astrocytes converged into accelerating directed motion. It follows that astrocyte migration to injury sites may be a key factor in the repair mechanisms orchestrated by FGF2.

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Section: Discussionmentioning

confidence: 99%

JNK/ERK/FAK Mediate Promigratory Actions of Basic Fibroblast Growth Factor in Astrocytes via CCL2 and COX2

Lichtenstein¹,

Madrigal

Pujol³

et al. 2012

Neurosignals

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“…The potential involvement of intercellular adhesion molecule-1 (ICAM-1 or CD54), a ligand of lymphocyte function-associated antigen-1 (LFA-1), in the interaction between CTL and target cells and thus in the regulation of CTL-mediated cytotoxicity has been well documented in a variety of studies (6)(7)(8). There is strong evidence that the engagement of LFA-1 on CTL by ICAM-1 on target cells is essential for T-cell activation and for directing the released of cytolytic granules into the tumor cells (9)(10)(11).…”

Section: Introductionmentioning

confidence: 99%

ICAM-1 Has a Critical Role in the Regulation of Metastatic Melanoma Tumor Susceptibility to CTL Lysis by Interfering with PI3K/AKT Pathway

et al. 2008

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Human primary melanoma cells (T1) were found to be more susceptible to lysis by a Melan-A/MART-1-specific CTL clone (LT12) than their metastatic derivative (G1). We show that this differential susceptibility does not involve antigen presentation by target cells, synapse formation between the metastatic target and CTL clone, or subsequent granzyme B (GrB) polarization. Although PI-9, an inhibitor of GrB, was found to be overexpressed in metastatic G1 cells, knockdown of the PI-9 gene did not result in the attenuation of G1 resistance to CTL-induced killing. Interestingly, we show that whereas T1 cells express high levels of intercellular adhesion molecule-1 (ICAM-1), a dramatically reduced expression was noted on G1 cells. We also showed that sorted ICAM-1 + G1 cells were highly sensitive to CTL-induced lysis compared with ICAM-1 À G1 cells. Furthermore, incubation of metastatic G1 cells with IFN-; resulted in the induction of ICAM-1 and the potentiation of their susceptibility to lysis by LT12. More importantly, we found that the level of ICAM-1 expression by melanoma cells correlated with decreased PTEN activity. ICAM-1 knockdown in T1 cells resulted in increased phosphorylation of PTEN and the subsequent activation of AKT. We have additionally shown that inhibition of the phosphatidylinositol (3,4,5)-triphosphate kinase (PI3K)/AKT pathway by the specific inhibitor wortmannin induced a significant potentiation of susceptibility of G1 and ICAM-1 small interfering RNA-treated T1 cells to CTLinduced lysis. The present study shows that a shift in ICAM-1 expression, which was associated with an activation of the PI3K/AKT pathway, can be used by metastatic melanoma cells to escape CTL-mediated killing. [Cancer Res 2008;68(23):9854-64]

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“…Among these alterations, an increase in expression of immediate-early response genes as well as different transcription factors in monocytes responding to injury or infection (21), an increase in c-myc protein levels in breast epithelial cells (22), a decrease in intercellular adhesion molecule-1 expression in lung cancer cells (23), the induction of matrix metalloproteinase gene expression (24), and >32 genes differentially modulated in salivary epithelial cells undergoing morphologic differentiation (25). Finally, expression of h 1 variants per se has been shown to increase p21 mRNA levels in hepatocellular carcinoma cells (26) or p27 kip1 levels (27) in several cell types and a V h 3 expression in LNCaP prostate cancer cells causes increased cdc2 mRNA, protein, and kinase activity levels (28).…”

Section: Introductionmentioning

confidence: 99%

β1 Integrins Modulate Cell Adhesion by Regulating Insulin-Like Growth Factor-II Levels in the Microenvironment

et al. 2006

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The interactions between cancer cells and the extracellular matrix (ECM) regulate cancer progression. The B 1C and B 1A integrins, two cytoplasmic variants of the B 1 integrin subfamily, are differentially expressed in prostate cancer. Using gene expression analysis, we show here that the B 1C variant, an inhibitor of cell proliferation, which is down-regulated in prostate cancer, up-regulates insulin-like growth factor-II (IGF-II) mRNA and protein levels. In contrast, B 1A does not affect IGF-II levels. We provide evidence that B 1C -mediated upregulation of IGF-II levels increases adhesion to Laminin-1, a basement membrane protein down-regulated in prostate cancer, and that the B 1C cytoplasmic domain contains the structural motif sufficient to increase cell adhesion to Laminin-1. This autocrine mechanism that locally supports cell adhesion to Laminin-1 via IGF-II is selectively regulated by the B 1 cytoplasmic domain via activation of the growth factor receptor binding protein 2-associated binder-1/SH2-containing protein-tyrosine phosphatase 2/phosphatidylinositol 3-kinase pathway. Thus, the concurrent local loss of B 1C integrin, of its ligand Laminin-1, and of IGF-II in the tumor microenvironment may promote prostate cancer cell invasion and metastasis by reducing cancer cell adhesive properties. It is, therefore, conceivable that reexpression of B 1C will be sufficient to revert a neoplastic phenotype to a nonproliferative and highly adherent normal phenotype. (Cancer Res 2006; 66(1): 331-42)

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Stimulation of be-ta1 integrin down-regulates ICAM-1 expression and ICAM-1 dependent adhesion of lung cancer cells through focal adhesion kinase

Cited by 21 publications

References 0 publications

JNK/ERK/FAK Mediate Promigratory Actions of Basic Fibroblast Growth Factor in Astrocytes via CCL2 and COX2

JNK/ERK/FAK Mediate Promigratory Actions of Basic Fibroblast Growth Factor in Astrocytes via CCL2 and COX2

ICAM-1 Has a Critical Role in the Regulation of Metastatic Melanoma Tumor Susceptibility to CTL Lysis by Interfering with PI3K/AKT Pathway

β1 Integrins Modulate Cell Adhesion by Regulating Insulin-Like Growth Factor-II Levels in the Microenvironment

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