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PubMed1998

Effect of high-dose electron beam irradiation on the migration of DOA and ATBC plasticizers from food-grade PVC and PVDC/PVC films, respectively, into olive oil.

The effect of high-dose irradiation on the migration of dioctyl adipate (DOA) and acetyl tributyl citrate (ATBC) plasticizers from food-grade poly (vinyl chloride) (PVC) and poly (vinylidene chloride/vinyl chloride) (PVDC/PVC) copolymer (Saran) films, respectively, into olive oil was studied. The results showed a significantly higher amount of DOA migrated into olive oil from irradiated versus nonirradiated samples. This difference was more noticeable in oil samples collected during initial periods of contact. The amount of DOA migrating into olive oil was lower for samples irradiated at a dose of 20 kGy in comparison with samples irradiated at a dose of 50 kGy. At a sampling time of 1 h the amount of DOA that migrated into olive oil was 93.9 mg/liter, 141.5 mg/liter, and 183.4 mg/liter for nonirradiated samples, 20-kGy irradiated samples, and 50-kGy irradiated samples, respectively. After 288 hr (12 days) of oil-film contact the respective amounts were 390.8 mg/liter, 409.2 mg/liter, and 430.1 mg/liter. There were no statistically significant differences in migrating amount of ATBC between nonirradiated samples and samples irradiated at a dose of 20 kGy, while in samples irradiated at a dose of 50 kGy the migration of ATBC was increased. After 1 h of oil-film contact no detectable amounts of ATBC had migrated. After 288 h of contact the amounts of ATBC that migrated into olive oil were 3.59 mg/liter, 3.56 mg/liter, and 4.12 mg/liter for nonirradiated samples, 20-kGy irradiated samples, and 50-kGy irradiated samples, respectively. It is suggested that plasticized PVC should not be used in direct contact with high-fat foodstuffs with or without irradiation treatment.

Adipates↗
PubMed1999

Glutamate acting at NMDA receptors stimulates embryonic cortical neuronal migration.

During cortical development, embryonic neurons migrate from germinal zones near the ventricle into the cortical plate, where they organize into layers. Mechanisms that direct neuronal migration may include molecules that act as chemoattractants. In rats, GABA, which localizes near the target destination for migrating cortical neurons, stimulates embryonic neuronal migration in vitro. In mice, glutamate is highly localized near the target destinations for migrating cortical neurons. Glutamate-induced migration of murine embryonic cortical cells was evaluated in cell dissociates and cortical slice cultures. In dissociates, the chemotropic effects of glutamate were 10-fold greater than the effects of GABA, demonstrating that for murine cortical cells, glutamate is a more potent chemoattractant than GABA. Thus, cortical chemoattractants appear to differ between species. Micromolar glutamate stimulated neuronal chemotaxis that was mimicked by microM NMDA but not by other ionotropic glutamate receptor agonists (AMPA, kainate, quisqualate). Responding cells were primarily derived from immature cortical regions [ventricular zone (vz)/subventricular zone (svz)]. Bromodeoxyuridine (BrdU) pulse labeling of cortical slices cultured in NMDA antagonists (microM MK801 or APV) revealed that antagonist exposure blocked the migration of BrdU-positive cells from the vz/svz into the cortical plate. PCR confirmed the presence of NMDA receptor expression in vz/svz cells, whereas electrophysiology and Ca2+ imaging demonstrated that vz/svz cells exhibited physiological responses to NMDA. These studies indicate that, in mice, glutamate may serve as a chemoattractant for neurons in the developing cortex, signaling cells to migrate into the cortical plate via NMDA receptor activation.

Animals↗
PubMed1999

Migradollars and mortality: the effects of migration on infant survival in Mexico.

We apply multilevel methods to data from Mexico to examine how village migration patterns affect infant survival outcomes in origins. We argue that migration is a cumulative process with varying health effects at different stages of its progression, and test several related hypotheses. Findings suggest higher rates of infant mortality in communities experiencing intense U.S. migration. However, two factors diminish the disruptive effects of migration: migradollars, or migrant remittances to villages, and the institutionalization of migration over time. Mortality risks are low when remittances are high and decrease as migration becomes increasingly salient to livelihoods of communities. Together, the findings indicate eventual benefits to all infants, irrespective of household migration experience, as a result of the development of social and economic processes related to U.S. migration.

Adult↗
PubMed1999

Regulation of human eosinophil migration across lung epithelial monolayers by distinct calcium signaling mechanisms in the two cell types.

In asthmatic patients, eosinophils massively infiltrate the lung tissues and migrate through lung epithelium into the airways. The regulatory mechanisms involved are obscure. We studied the role of calcium in the migration of human eosinophils across monolayers of human lung epithelial H292 cell line cells induced by combined chemotactic solutions of platelet-activating factor and C5a. The transepithelial migration of eosinophils was attenuated by depletion of the external Ca2+ in the migration system, whereas the eosinophil migration itself was unaffected as evidenced by measuring eosinophil chemotaxis in the Boyden chamber in the absence of epithelial cells. Buffering of intracellular Ca2+ in eosinophils with 1, 2-bis(o-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid tetra(acetoxymethyl) ester (BAPTA/AM) inhibited both eosinophil transepithelial migration and eosinophil chemotaxis in the Boyden chamber, suggesting the importance of intracellular Ca2+ in eosinophil transmigration. Although loading of BAPTA/AM or addition of thapsigargin to the epithelial cells effectively changed their cytoplasmic free Ca2+ concentrations, neither of these treatments affected transepithelial migration of eosinophils. Interestingly, addition of La3+ (0.2 mM) to epithelial cells suppressed eosinophil transmigration whereas addition of La3+ to eosinophils did not. Taken together, these results show the importance of Ca2+ in eosinophil migration across lung epithelium and support a distinctive regulatory role of intracellular and extracellular Ca2+ for the two cell types involved in this process; i.e., the transmigration of human eosinophils across a monolayer of lung epithelial cells is regulated by the intracellular Ca2+ in eosinophils, whereas the ability of the lung epithelial cell monolayer to allow eosinophil passage is dependent on the extracellular Ca2+.

Buffers↗
PubMedDate not supplied

Induction of transendothelial migration in normal and malignant human T lymphocytes.

Activated CD 3+ enriched human peripheral blood T cells exhibited potent capacity for transendothelial migration through HUVEC layers in the absence of T cell ***. In contrast, malignant human T cell lines *** no or negligible ability of transendothelial migration in the absence of chemoattractants. Time lapse studies of transendothelial migration of activated CD 3+ enriched peripheral blood T cells through a HUVEC layer showed that the first T cells were detected in the lower compartment of a tissue culture insert after 1 hour and that migration increased to reach a maximum of 25 x 10(4) T cells/hr after 24 hours. Adhesion assays of human T cell lines demonstrated that all T cell lines were capable of adhesion to HUVEC and that adhesion of T cells to HUVECs was primarily mediated by CD11a/CD18 and ICAM-1 interactions. Furthermore, transendothelial migration of CD 3+ enriched human peripheral blood T cells was inhibited by pretreating the T cells with anti-CD 18 monoclonal antibodies. The inability of malignant T cells to migrate through HUVEC layers in the absence of chemoattractants was not due to poor motility per se, since both normal and malignant T cells migrated well on extracellular matrix components as determined by using Boyden chambers. Crosslinking of alpha 1 beta 2 and alpha 4 beta 1 with immobilized monoclonal antibodies induced motile behaviour in activated CD 3 enriched human peripheral blood T cells but not in malignant T cell lines. In conclusion, the differences in the ability of transendothelial migration between normal and malignant human T cells in the absence of chemoattractants is primarily due to the differences in the capacity of alpha 1 beta 2 and alpha 4 beta 1 to trigger motile behaviour in the separate cell types.

Adult↗
PubMed2000

Promotion of adhesion and migration of RPE cells to provisional extracellular matrices by TNF-alpha.

PURPOSE: Adhesion and migration of retinal pigment epithelial (RPE) cells to provisional extracellular matrices (ECM) is important in the development of epiretinal membranes found in proliferative vitreoretinopathy (PVR). Tumor necrosis factor alpha (TNF-alpha) is found in PVR membranes and regulates many functions of RPE cells. In this study, the effects of TNF-alpha on adhesion and migration of RPE cells to various components of ECM were examined and elucidation of the mechanism of the response was attempted. METHODS: Mitogen activated protein kinase (ERK1/2; MAPK) activation was measured by immunoblot. RPE cells pretreated with TNF-alpha (10 ng/ml) or TNF-alpha + PD98059 (a specific inhibitor of MAPK, 30 microM) for 24 hours were compared with control RPE. Attachment was measured by modified MTT assay on fibronectin and collagen types I and IV. Spreading was measured by staining with fluo3-AM and confocal laser scanning microscopy. Migration of RPE cells on substrates was determined by Boyden chamber assay using PDGF-BB (20 ng/ml) as a chemotactic factor. Integrin expression was determined by flow cytometry and RT-PCR. RESULTS: TNF-alpha rapidly activated MAPK and increased the extent of attachment, spreading and migration on fibronectin and collagen type I (P < 0.01) but not on collagen type IV. TNF-stimulated RPE cells showed increased mRNA and surface protein expression for alpha1 and alpha5 integrin (P < 0.01) but not alpha3 integrin subunit. Neutralizing the anti-alpha1 antibody inhibited migration on collagen type I, whereas alpha5 antibody inhibited fibronectin-induced migration. Treatment with both TNF and PD98095 reduced attachment and migration on provisional ECM and reduced the upregulated integrin expression to control levels. CONCLUSIONS: After treatment with TNF-alpha, there is increased expression of specific integrins associated with increased adhesion and migration on provisional ECM (fibronectin and collagen type I). This effect is mediated, at least in part, by activation of MAPK signaling pathway.

Calcium-Calmodulin-Dependent Protein Kinases↗
PubMed2000

Smooth muscle cell migration promoting activity of plasma predicts restenosis in patients with peripheral arterial occlusive disease undergoing angioplasty.

BACKGROUND: Efficacy of percutaneous transluminal angioplasty (PTA) is limited by restenosis occurring in a large proportion of patients. Smooth muscle cell (SMC) migration is a major pathomechanism of restenosis. We studied SMC migration inducing activity of plasma from patients with peripheral arterial occlusive disease (PAOD) undergoing PTA. METHODS AND RESULTS: SMC migration was determined in a two-dimensional assay system after addition of 1/25 plasma dilutions. Mean increase in migration area was 65.5 +/- 33.8% in normal controls and 67.7 +/- 53.2% in patients with PAOD. 6 hours after PTA, plasmatic migration inducing activity was largely unchanged. In 19/30 patients with restenosis (6 months after PTA) migration promoting activity (82.7 +/- 60.0) was significantly higher than in 11/30 patients with patent vessels (41.8 +/- 21.0; p = 0.03). No correlation of clinical risk factors with outcome was observed. A weak correlation was found between plasmatic migration promoting activity and levels of epidermal growth factor and transforming growth factor-beta. CONCLUSION: The capacity of human plasma to stimulate SMC migration in tissue culture can be used to assess the risk for restenosis after PTA in patients with PAOD.

Aged↗
PubMed2001

Role of the small GTP-binding protein rho in epithelial cell migration in the rabbit cornea.

PURPOSE: To determine the role of the small guanosine triphosphate (GTP)-binding protein Rho in the migration of corneal epithelial cells. METHODS: The presence of the Rho target proteins Rho-associated coiled coil-containing protein kinase (ROCK)-1 and ROCK-2 in rabbit cornea was examined by immunohistochemical analysis, and that of the corresponding mRNAs in rabbit corneal epithelial cells was determined by reverse transcription-polymerase chain reaction analysis. The effects of various agents on epithelial cell migration were investigated by measuring the length of the migration path in rabbit corneal blocks in culture. RESULTS: Both ROCK-1 and ROCK-2 were detected in the rabbit corneal epithelium at both protein and mRNA levels. The Rho activator lysophosphatidic acid (LPA) stimulated corneal epithelial migration in a dose-dependent manner, whereas exoenzyme C3, a Rho inhibitor, inhibited epithelial migration also in a dose-dependent manner. The stimulatory effect of LPA on corneal epithelial migration was prevented by exoenzyme C3. Both cytochalasin B, an inhibitor of actin filament assembly, and ML-7, an inhibitor of myosin light chain kinase, also prevented LPA stimulation of epithelial migration. CONCLUSIONS: These results suggest that Rho mediates corneal epithelial migration in response to external stimuli by regulating the organization of the actin cytoskeleton.

Actins↗
PubMed2002

FAK-mediated inhibition of vascular smooth muscle cell migration by the tetraspanin CD9.

Migration of vascular smooth muscle cells (SMC) towards the intima is a key event in vascular proliferative diseases. We investigated a potential role for the tetraspanin CD9 in this process in a wound migration assay. Aortic SMC from CD9 knock-out mice had higher migration rates and the presumably stimulatory anti-CD9 antibody ALMA-1 inhibited migration of human SMC. The signaling pathways responsible for this inhibitory effect were investigated. In migrating CD9-/- SMC, stress fiber formation was decreased and focal adhesions were smaller and more diffusely distributed, consistent with an inhibition of integrin clustering. In migrating mouse SMC expressing CD9, focal adhesion kinase (FAK) tyrosine phosphorylation was doubled. No differences in intracellular calcium signaling were observed between CD9+/+ and CD9-/- SMC during migration. We suggest that CD9 in hibits SMC migration by a stimulation of both stress fiber formation and integrin clustering, leading to a stimulation of FAK phosphorylation.

Actins↗
PubMed2002

Direct comparison of the migration of three cell types involved in epiretinal membrane formation.

PURPOSE: The purpose of the present study was to develop an accurate and sensitive migration assay to compare the migratory capabilities of retinal pigment epithelial (RPE) cells, retinal glial (RG) cells, and fibroblasts (the cell types crucial in epiretinal membrane [ERM] formation) under identical microenvironmental conditions and thus to identify potential target areas in ERM management. METHODS: Cultured bovine RPE and RG cells and scleral fibroblasts (SFs) in both single and mixed cell type populations were induced to migrate in modified 48-well Boyden chambers. The labels used to distinguish between the cell types were latex microspheres and carmine particles. The chemoattractants used were fibronectin and PDGF, both of which are associated with epiretinal membrane development. RESULTS: When migrating independently, all three cell types showed a positive response to fibronectin at an optimal concentration of 10 microg/mL. The RG cells migrated in a significantly greater number than the RPE cells (P < 0.05), but the differences in number of migrating cells between RG cells and SFs and RPE cells and SFs were not significant. When the cells were labeled and migrating together, it became clear that the RG cells consistently migrated in a higher number than the SFs (P <or= 0.001) and both the SFs and RG cells showed a greater migratory response than the RPE cells (P <or= 0.01). CONCLUSIONS: The mixed cell migration (MCM) test system is a simple and useful assay to distinguish between the migratory responses of different cell types in the same microenvironment. It has highlighted the pronounced migratory response of RG cells to standard chemoattractants and has cast some level of doubt that, in comparative migratory terms, RPE cells are particularly good responders.

Animals↗
PubMed2002

Normal and abnormal neuronal migration in the developing cerebral cortex.

Neuronal migration is the critical cellular process which initiates histogenesis of cerebral cortex. Migration involves a series of complex cell interactions and transformation. After completing their final mitosis, neurons migrate from the ventricular zone into the cortical plate, and then establish neuronal lamina and settle onto the outermost layer, forming an "inside-out" gradient of maturation. This process is guided by radial glial fibers, requires proper receptors, ligands, other unknown extracellular factors, and local signaling to stop neuronal migration. This process is also highly sensitive to various physical, chemical and biological agents as well as to genetic mutations. Any disturbance of the normal process may result in neuronal migration disorder. Such neuronal migration disorder is believed as major cause of both gross brain malformation and more special cerebral structural and functional abnormalities in experimental animals and in humans. An increasing number of instructive studies on experimental models and several genetic model systems of neuronal migration disorder have established the foundation of cortex formation and provided deeper insights into the genetic and molecular mechanisms underlying normal and abnormal neuronal migration.

1-Alkyl-2-acetylglycerophosphocholine Esterase↗
PubMedDate not supplied

[In vitro migration activity of human peripheral blood neutrophils in the normal state and in immunopathology].

Methodological approaches to evaluation of the migration activity of human peripheral blood neutrophils into a collagen matrix were worked out. The migration of neutrophils in healthy donors and in patients with severe bronchial asthma was studied. In the normal state there was practically no migration of intact neutrophils into the collagen matrix (1.1 +/- 0.4%). Following their stimulation by formyi peptide about a quarter of their population was drawn into the matrix in avalanche (22.0 +/- 5.9%). In the acute phase of severe bronchial asthma an increase in both spontaneous (3.3 +/- 1.5%, P < 0.01) and stimulated (35.6 +/- 4.6%, P < 0.001) cell migration occurred. Changes in the migration characteristics of the neutrophils of patients and those of the cells of healthy donors, treated with the polycytokine preparation at concentrations exceeding 100 g/ml, followed similar trends. In case of the standard asthma treatment along with positive disease dynamics further increase in spontaneous neutrophil migration (5.8 +/- 2.9%, P < 0.001) in combination with deficiency in cells reaction to formyi peptide (11.8 +/- 3.8%, P < 0.01) was registered. At the same time dexamethasone did not change the character of the in vitro migration of neutrophils into the collagen matrix. Thus the dynamics of the peripheral blood neutrophil migration during treatment of severe bronchial asthma was demonstrated; this dynamics could be indicative of the pathogenetic role of neutrophils in the development of this pathology.

Acute-Phase Reaction↗
PubMed2003

Membrane type-1-matrix metalloproteinase expressed by prostate carcinoma cells cleaves human laminin-5 beta3 chain and induces cell migration.

Degradation of the extracellular matrix by proteolytic enzymes is a central aspect of physiological and pathologic tissue-remodeling processes such as trophoblastic implantation, wound healing, and tumor invasion. We have hypothesized that prostate adenocarcinoma cell invasion through the normal basal lamina is attributable in part to metalloproteinase-induced cleavage of laminin-5 (Ln-5) and enhanced motility of the cancer cells. We studied the role of membrane type-1-matrix metalloproteinase (MT1-MMP) expressed on the surface of prostate tumor cells in cleaving Ln-5 and enhancing the migration of prostate tumor cells. We also determined the nature of the MT1-MMP cleavage of human Ln-5 and how this altered Ln-5 changes the migration of prostate carcinoma cells. We found that human MT1-MMP cleaves purified human Ln-5 to an 80-kDa fragment. Mass spectrometry analyses of the 80-kDa cleaved product by trypsin and chymotrypsin gave 14 and 9 different peptide sequences, respectively, that were identical to the expected amino acid sequence of the Ln-5-beta3 chain. The recovered peptides represent 14.4% (trypsin) and 10.3% (chymotrypsin) of Ln-5-beta3 chain by amino acid count. Both trypsin and chymotrypsin digestion of MT1-MMP-cleaved product of Ln-5 did not show any other peptides that were identical to the other chains of Ln-5. Using a linear migration assay we found that the Ln-5 cleaved by MT1-MMP enhanced the migration of DU-145 prostate carcinoma cells by 2-fold compared with uncleaved Ln-5. The use of blocked antisense MT1-MMP oligonucleotides inhibited the migration of DU-145 cells on Ln-5. We also found that the prostate carcinoma cells expressing high levels of MT1-MMP, such as PC3N and PPC, demonstrated enhanced migration on human Ln-5-coated substrate, and this migration was inhibited using blocked antisense MT1-MMP oligonucleotides. In conclusion, this is a novel and important finding where we have shown that beta3-chain is cleaved by MT1-MMP, and this cleavage enhances migration of prostate cancer cells.

Amino Acid Sequence↗
PubMed1992

Independent modulation of enterocyte migration and proliferation by growth factors, matrix proteins, and pharmacologic agents in an in vitro model of mucosal healing.

BACKGROUND: Gastrointestinal mucosa heals by restitution and proliferation. These are difficult to distinguish in vivo. METHODS: Human Caco-2 enterocytes were cultured on matrix proteins (collagen I, laminin, fibronectin) with growth factors (epidermal growth factor [EGF] and transforming growth factor-beta 1 [TGF-beta 1]) and the tyrosine kinase and prostaglandin inhibitors genistein and indomethacin. Healing was modeled by means of monolayer expansion, proliferation by means of 3H-thymidine uptake, and restitution by means of mitomycin-blocked migration. RESULTS: Changing matrix composition failed to alter proliferation, but collagen I stimulated migration more than laminin or fibronectin (laminin/collagen, 68% +/- 2%; p less than 0.05). EGF (30 ng/ml) increased proliferation on both collagen (225% +/- 11% of basal) and laminin (206% +/- 26%) but increased migration only over laminin (210% +/- 17%) (all, p less than 0.05). TGF-beta 1 (200 pg/ml) stimulated migration over laminin (187% +/- 18%, p less than 0.005) but inhibited migration over collagen (89% +/- 3%, p less than 0.01) and did not affect 3H-thymidine uptake. When cultured on laminin, EGF but not TGF-beta 1 altered organization of the alpha 2 integrin subunit. Genistein (100 mumol/L) inhibited basal and EGF-stimulated 3H-thymidine uptake. In addition, it prevented EGF stimulation of replication-blocked migration (81% +/- 10% vs 190% +/- 20% of basal, p less than 0.0001) without altering basal replication-blocked migration. Indomethacin (10(-5) mol/L) did not alter migration but inhibited basal and EGF-stimulated proliferation by 7% +/- 1% (each, p less than 0.005). CONCLUSIONS: Restitution and proliferation appear independently regulated by matrix and growth factors. It may be possible to individually target specific phases of mucosal healing by means of pharmacologic agents.

Cell Division↗
PubMedDate not supplied

Inositol hexaphosphate (IP6) inhibits key events of cancer metastasis: I. In vitro studies of adhesion, migration and invasion of MDA-MB 231 human breast cancer cells.

BACKGROUND: The anti-cancer agent inositol hexaphosphate (IP6) is an abundant intrinsic component of both plant and mammalian cells. In addition to inducing differentiation and inhibiting growth of numerous cancer cell lines in vitro, IP6 has been demonstrated to prevent and abrogate both primary tumor and metastasis in vivo. MATERIALS AND METHODS: Using MDA-MB 231 human breast cancer cells, we studied the potential of IP6 to inhibit cell adhesion, migration and invasion, the key steps in cancer metastasis, utilizing the extracellular matrix (ECM) proteins, a culture wounding assay, modified Boyden chambers, immunocytochemistry and zymography. RESULTS: IP6 treatment caused a 65% reduction of cell adhesion to fibronection (p = 0.002) and a 37% reduction to collagen (p = 0.005). To determine whether a decrease in cell adhesion leads to a decrease in cell motility, migration assays were performed; IP6 decreased both the number of migrating cells and the distance of cell migration into the denuded area by 72% (p < 0.001). Haptotatic cell migration in a modified Boyden chambers was also reduced in a dose-dependent manner. While cell migration on fibronectin was inhibited by 65% (p < 0.001), migration on collagen and laminin was decreased by 32% (p < 0.01) and 13% (p < 0.05), respectively. Immunocytochemistry revealed the absence of lamellipodia structure in IP6-treated cells as compared to untreated cells, corresponding to a diminished ability of cancer cells to form cellular network as determined by Matrigel outgrowth assay. Likewise, cell invasion also was decreased (by 72% after IP6 treatment, p = 0.001) in a dose-dependent fashion. Additionally, IP6 significantly (p = 0.006) inhibited the secretion of matrix metalloproteinase (MMP)-9 as assessed by zymography. CONCLUSION: The results of this study show that IP6 inhibits the metastasis of human breast cancer cells in vitro through effects on cancer cell adhesion, migration and invasion.

Breast Neoplasms↗
PubMed2004

CXCR4 antagonist inhibits stromal cell-derived factor 1-induced migration and invasion of human pancreatic cancer.

The stromal cell-derived factor-1 (SDF-1)/CXCR4 system is implicated in various instances of cell migration in mammals, including the migration of lymphocytes and the formation of metastases. We have recently synthesized a potent novel CXCR4 antagonist, TN14003. The purpose of this study was to investigate the role of SDF-1/CXCR4 axis in the pancreatic cancer metastasis via cell migration and invasion, and the inhibitory effect of TN14003 on pancreatic cancer cell metastasis. The expression of CXCR4 was detected in six pancreatic cancer cell lines by Western blotting and immunocytochemistry. In migration and invasion assays, SDF-1 stimulated both migration and invasion of cancer cells in a dose-dependent manner. The maximal effect of SDF-1 was observed at 100 ng/ml. SDF-1-induced migration and invasion of cancer cells were completely blocked by 100 nM TN14003. The stimulatory effect of SDF-1 on cancer migration and the inhibitory effect of TN14003 were mediated via the alteration in phosphorylation of mitogen-activated protein kinases. Treatment of cancer cells with 100 ng/ml SDF-1 resulted in a significant increase of actin polymerization, which was reduced by 100 nM TN14003. SDF-1 enhanced cancer cell adhesion to laminin, which was not reversed by TN14003. Taken together, SDF-1/CXCR4 axis is involved in pancreatic cancer metastasis through migration and invasion. The small molecule antagonists against CXCR4 such as TN14003 might be an effective anti-metastatic agent for pancreatic cancer.

Actins↗
PubMed2004

[Dynamic changes in focal adhesion kinase during cell migration induced by bFGF and the significance].

Cell migration plays an important role in repair of injury, angiogenesis, cancer metastasis and so on. In this paper the effects of basic fibroblast growth factor (bFGF) of different concentrations on ECV-304 cell migration, and the dynamic changes in focal adhesion kinase (FAK) were observed. The relationship between FAK and cell migration induced by bFGF was studied. A ECV-304 cell scratch wound model was established and the images of cell migration were quantitatively measured using a computer-assisted videomicroscopic system. The dynamic changes in FAK content (Western blot), FAK activity (immunoprecipitation plus Western blot) and FAK mRNA (RT-PCR) were measured in vitro. The expression of integrin alpha3 was investigated using immunocytochemical staining (ABC method). The results showed that bFGF produced a dual-phase regulatory effect on ECV-304 migration when the cell confluent areas reached 90%-95% in culture. It was found that compared with the control group (0 ng/ml bFGF), the cell migration was stimulated (P<0.05), inhibited (P<0.05) and unchanged when the cultured cells were treated with bFGF at the concentrations of 5, 10 and 15 ng/ml, respectively. The content and activity of FAK protein were markedly up-regulated in 5 ng/ml bFGF group and down-regulated in 15 ng/ml bFGF group, respectively. FAK mRNA expression came to the peak in 5 ng/ml bFGF group after 6 h culture and there was a significant difference compared with the control group. In various experimental groups there were no significant differences in the expression of integrin alpha3 compared with the control group according to the immunocytochemical staining. The results mentioned above suggest that different concentrations of bFGF have a dual-phase effect on the migration of cultured ECV-304 cells, which correlates positively with FAK content, activity and mRNA in cultured ECV-304 cell scratch wound model. The FAK plays an important role in the signal transduction pathway of cell migration induced by bFGF, while bFGF can regulate the content of FAK in ECV-304 cells at gene transcription level.

Cell Movement↗
PubMedDate not supplied

Effects of migration on cancer incidence and resources for prevention and treatment in Florida.

Migration adds a complex dimension to the task of those who plan and allocate resources for health care. The authors offer a methodology for estimating the contribution of migration to the incidence of cancer, allow for age- and sex-specific cancer risks, and estimate, by country, the impact of recent migration on the annual incidence of cancer in Florida. Cancer and migration data were used to develop estimates of the number of cancer cases for Florida counties that were attributable to recent migrants. A net gain and loss ratio was calculated for new cancer cases in 1980 resulting from the 1975-80 migration pattern. Florida data was used because that State has one of the highest crude cancer incidence rates in the nation, is one of the most populous States, and has a population growth from migration rather than from natural increase. Preliminary findings on the relationship between cancer health services resources and net cancer rates from migration are discussed. County cancer health services resources had a strong positive relationship to population size, but the impact of migration on cancer incidence was in a curvilinear relationship to population size.

Cancer Care Facilities↗