Biomedical subjects

Qiang Yu

Publications and source records attributed to Qiang Yu.

At least 37 records · Page 2Linked to original sources

PubMed2004

Sodium 4-phenylbutyrate induces apoptosis of human lung carcinoma cells through activating JNK pathway.

Sodium 4-phenylbutyrate (PB) has been used in the therapy of urea cycle defects for many years. Recently, it has been shown to cause cellular differentiation, growth arrest, and apoptosis in certain malignancies. We have analyzed the effects of PB on human lung carcinoma cells. PB has distinct patterns of effects on different lung carcinoma cells, inducing apoptosis in NCI-H460 and NCI-H1792 cells, causing G1 arrest in A549 and SK-LU-1 cells, but having no effect on a non-transformed bronchial epithelial cell line HBE4-E6/E7. We investigated the role of MAP kinase family members, extracellular signal-regulated kinase (ERK), JNK, and p38 mitogen-activated protein kinase (MAPK), as well as other important cell survival signaling molecules in PB-induced apoptosis. We observed activation of JNK and ERK by PB in the lung cancer cells. JNK was activated only in the two apoptotic cells, whereas ERK was activated in both the apoptotic and the growth-arrested cells, demonstrating a correlation between apoptosis and activation of JNK in response to PB. Both JNK inhibitor and JNK RNA interference (RNAi) inhibited PB-induced apoptosis, whereas MEK inhibitor did not, supporting that apoptosis induced by PB is through activation of JNK. De novo protein synthesis is required for the PB-induced JNK activation and induction of apoptosis. However, the production of known upstream activators of JNK, namely Fas/Fas ligand, tumor necrosis factor (TNF)-alpha, TNF-beta, and TRAIL, are not altered by PB treatment. Therefore, PB activates JNK through an unidentified and cell type-specific mechanism. Understanding of this mechanism is of therapeutic value in treating cancer patients with PB.

Adenocarcinoma↗

PubMed2004

Susceptibility to cell death induced by blockade of MAPK pathway in human colorectal cancer cells carrying Ras mutations is dependent on p53 status.

Constitutive activation of mitogen-activated protein kinase (MAPK) pathway is implicated in a variety of human malignancies especially those that carry Ras mutations and is currently exploited as a cancer therapeutic target. The variability of response by cancer cells to the inhibition of the Ras/MAPK pathway both in vivo and in vitro, however, suggests that the genetic background of the tumor cell may modulate the effectiveness of this directed therapeutic. In a panel of colorectal cancer cell lines that carry Ras mutations and have constitutively active MEK/MAPK, we found that inhibition of the MAPK upstream kinase MEK by the small molecular MEK inhibitor U0126 induced cell death only in p53 wild-type cells. By contrast, p53-deficient cells were not affected by blocking the MEK/MAPK pathway. Using isogenic colon cancer cell lines and RNA interference, we show that loss of p53 significantly reduces MAPK phosphorylation and renders cells resistant to U0126 treatment. These findings reveal a critical role for p53 in MAPK-driven cell survival and place p53 upstream in the control cascade of MAPK activity. The therapeutic implication of these observations is that MAPK inhibitors will be most beneficial as a therapeutic agent in p53 normal colon cancers where constitutively active MAPK resulting from a Ras mutation is required for cell survival.

Apoptosis↗

PubMed2004

p53-regulated transcriptional program associated with genotoxic stress-induced apoptosis.

By using a genome-wide approach, we sought the identification of p53-regulated genes involved in cellular apoptosis. To this end, we assessed the transcriptional response of HCT116 colorectal cancer cells during apoptosis induced by the anticancer drug 5-fluorouracil as the function of p53 status, and we identified 230 potential targets that are regulated by p53. Previously identified p53 targets known to be involved in growth arrest and apoptosis were observed to be induced, thus validating the approach. Strikingly, we found that p53 regulates gene expression primarily through transcriptional repression (n = 189) rather than activation (n = 41), and selective blockade of p53-dependent gene repression resulted in the reduction in 5-fluorouracil-induced apoptosis. Reporter and chromatin immunoprecipitation assays demonstrated that p53 can suppress the promoter activities of three further studied candidate genes PLK, PTTG1, and CHEK1 but would only bind directly to PTTG1 and CHEK1 promoters, revealing that p53 can repress gene expression through both direct and indirect mechanisms. Moreover, RNA(i)-mediated knockdown of PLK and PTTG1 expression was sufficient to induce apoptosis, suggesting that repression of novel anti-apoptotic genes by p53 might contribute to a significant portion of the p53-dependent apoptosis. Our data support the divergent functions of p53 in regulating gene expression that play both synergistic and pleiotropic roles in p53-associated apoptosis.

Apoptosis↗

PubMed2004

Simulation of the stomatal conductance of winter wheat in response to light, temperature and CO2 changes.

BACKGROUND AND AIMS: The stomata are a key channel of the water cycle in ecosystems, and are constrained by both physiological and environmental elements. The aim of this study was to parameterize stomatal conductance by extending a previous empirical model and a revised Ball-Berry model. METHODS: Light and CO(2) responses of stomatal conductance and photosynthesis of winter wheat in the North China Plain were investigated under ambient and free-air CO(2) enrichment conditions. The photosynthetic photon flux density and CO(2) concentration ranged from 0 to 2000 micro mol m(-2) s(-1) and from 0 to 1400 micro mol mol(-1), respectively. The model was validated with data from a light, temperature and CO(2) response experiment. RESULTS: By using previously published hyperbolic equations of photosynthetic responses to light and CO(2), the number of parameters in the model was reduced. These response curves were observed diurnally with large variations of temperature and vapour pressure deficit. The model interpreted stomatal response under wide variations in environmental factors. CONCLUSIONS: Most of the model parameters, such as initial photon efficiency and maximum photosynthetic rate (P(max)), have physiological meanings. The model can be expanded to include influences of other physiological elements, such as leaf ageing and nutrient conditions, especially leaf nitrogen content.

Carbon Dioxide↗

PubMed2004

Distinctive regulation and function of PI 3K/Akt and MAPKs in doxorubicin-induced apoptosis of human lung adenocarcinoma cells.

Regulation and function of PI 3K/Akt and mitogen-activated protein kinases (MAPKs) in doxorubicin-induced cell death were investigated in human lung adenocarcinoma cells. Doxorubicin induced dose-dependent apoptosis of human lung adenocarcinoma NCI-H522 cells. Prior to cell death, both Akt and the MAPK family members (MAPKs: ERK1/2, JNK, and p38) were activated in response to the drug treatment. The kinetics of the inductions for Akt and MAPKs are, however, distinct. The activation of Akt was rapid and transient, activated within 30 min of drug addition, then declined after 3 h, whereas the activations of three MAPKs occurred later, 4 h after addition of the drug and sustained until cell death occurred. Inhibition of PI 3K/Akt activation had no effect on MAPKs' activation, suggesting that the two pathways are independently activated in response to the drug treatment. Inhibition of PI 3K/Akt and p38 accelerated and enhanced doxorubicin-induced cell death. On the contrary, inhibition of ERK1/2 or JNK had no apparent effect on the cell death. Taken together, these results suggest that PI 3K/Akt and MAPKs signaling pathways are all activated, but with distinct mechanisms, in response to doxorubicin treatment. Activation of PI 3K/Akt and p38 modulates apoptotic signal pathways and inhibits doxorubicin-induced cell death. These responses of tumor cells to cancer drug treatment may contribute to their drug resistance. Understanding of the mechanism and function of the responses will be beneficial for the development of novel therapeutic approaches for improvement of drug efficacy and circumvention of drug resistance.

Adenocarcinoma↗

PubMed2004

Cleavage of p130Cas in anoikis.

p130Cas is a multifunctional signaling adaptor protein. It integrates and relays signals generated from a variety of extracellular stimuli and regulates a number of cellular activities including cell death. In this study, we analyzed the regulation and function of p130Cas in anoikis, a type of apoptosis caused by disruption of cell-matrix interactions. We found that p130Cas was specifically cleaved during anoikis in anoikis-sensitive epithelial cells, but not in anoikis-resistant tumor cells. There is a close correlation between p130Cas cleavage and anoikis. Furthermore, we found that the cleavage of p130Cas, as well as another focal adhesion component FAK, is different from that of caspase substrate PARP and spectrin. Although caspases and calpain were found to be involved in the cleavage of p130Cas, there appear to be other unidentified proteases that are mainly responsible for the cleavage of p130Cas, particularly at the early stage of anoikis. Overexpression of the p130Cas cleavage product induced apoptosis. Taken together, these data suggest that there are novel proteases involved in the cleavage of p130Cas during anoikis, which may be functionally involved in the onset of anoikis. p130Cas may have a dual role in the regulation of anoikis. On one hand, it mediates a survival signal from cell-matrix interactions when cells are attached to the extracellular matrix. On the other hand, it participates in executing cell death when cell-matrix interactions are disrupted. These observations provide new insights into the understanding of the function of p130Cas and the molecular mechanism of anoikis.

Animals↗

PubMed2004

CT features of synovial chondromatosis in the temporomandibular joint.

OBJECTIVE: The purpose of this study was to determine the characteristic computed tomography (CT) findings of synovial chondromatosis of the temporomandibular joint (TMJ). STUDY DESIGN: Eight subjects with synovial chondromatosis were examined with axial and coronal CT scans. All lesions were histopathologically confirmed either through an arthroscopic punch biopsy or surgery. CT appearances of the lesions were reviewed and classified. RESULTS: Among the 8 subjects, 7 (87.5%) demonstrated soft tissue swelling, 7 (87.5%) showed loose calcified bodies, and 6 (75%) had bony changes of the articular surfaces. Patterns of the skull base changes as well as intracranial extension of the disease were identified. CONCLUSIONS: Based on the CT findings, synovial chondromatosis of the TMJ is characterized by soft tissue swelling, loose calcified bodies, and bony changes of the skull base. The latter may lead to destruction of the central skull base and intracranial extension.

Adult↗

PubMed2004

Study of the PTEN gene expression and FAK phosphorylation in human hepatocarcinoma tissues and cell lines.

The tumor suppressor PTEN gene maps to chromosome 10q23.3 and encodes a dual specificity phosphatase. Mutations of this gene had been found in a variety of human tumors. In the present study, we analyzed the structure and expression of the PTEN gene in 34 hepatocellular carcinoma tissues and two hepatoma cell lines. We found neither homozygous nor hemizygous deletions in these samples. We, however, found point mutations in 4 of the 34 tissue samples. Five of ten hepatocellular carcinoma tissues showed reduced PTEN expression at mRNA level. HepG2 and SMMC-7721 hepatoma cells showed decreased PTEN expression at both mRNA and protein levels compared with immortalized L02 hepatic cells. PTEN mRNA in SMMC-7721 hepatoma cells could be reduced by TGF-betaI treatment. We also found that the phosphorylation levels of FAK in both of the hepatoma cell lines were higher than that in L02 hepatic cells. Transient expression of the PTEN gene in SMMC-7721 and HepG2 hepatoma cells resulted in decreased FAK phosphorylation. The level of FAK tyrosine phosphorylation appeared to be inversely correlated with the level of the PTEN protein. In summary, our results indicated that the function of the PTEN gene in hepatocarcinomas may be impaired mainly through point mutations and expression deficiency and that the defect of PTEN in tumor cells could alter the phosphorylation of FAK.

Base Sequence↗

PubMed2004

[Relationship between protein tyrosine phosphorylation level and anoikis resistance of breast tumor cell lines].

BACKGROUND & OBJECTIVES: Normal epithelial or endothelial cells can undergo anoikis, a type of apoptosis, when they are detached from their extracellular matrices (ECM), while most tumor cells derived from epithelial or endothelial tissues lose this feature. Most of the studies indicate that anoikis resistance of tumor cells is closely related to abnormal signal transductioin. The aim of this research was to screen out the tumor cell lines that are anoikis resistant, then to investigate the relationship between the protein tyrosine phosphorylation of signaling molecules and anoikis resistance feature of tumor cells. METHODS: Anoikis resistance of breast tumor cell lines MCF-7, Bcap-37, and MDA-MB-231 was determined by DNA ladder assay, flow cytometry analysis, and soft agar assay upon suspending culture. A normal epithelial cell line MDCK (Madin-Darby canine kidney) was taken as a control. The inhibitory effect of genistein, a general protein tyrosine kinase inhibitor, on anoikis resistance of tumor cells was analyzed at the same time. The differences of total protein tyrosine phosphorylation levels between suspended and attached cultural conditions of three breast cancer cell lines were examined by Western blot analysis. RESULTS: All the three tumor cell lines were distinctly anoikis resistant. Further study showed that these features could be suppressed by genistein. The results of Western blot analysis showed that the general level of tyrosine phosphorylation in suspended MDCK cells was decreased compared with that in attached cells, while tyrosine phosphorylation level of some proteins increased (more than 3.5-6.5 folds) aberrantly in suspended tumor cells. CONCLUSION: All the three breast tumor cells in this study are anoikis resistant respectively to some extent, and aberrant tyrosine phosphorylation of signaling proteins may play a role in the process of anoikis resistance of these tumor cells.

Animals↗

PubMed2004

[CT imaging analysis in 138 cases with orbital fractures].

PURPOSE: To investigate CT findings of orbital fractures in maxillofacial injuries in order to improve clinical diagnostic accuracy. METHODS: CT findings of 138 cases (145 orbits) with orbital fractures in maxillofacial injuries were analyzed. RESULTS: In maxillofacial injuries, orbital fractures of medial and posterolateral walls were most common,which often showed multiple walls fractures. In 145 orbital fractures, there were single wall fractures in 51 cases (35.17%), two-wall fractures in 48 cases (33.10%), three-wall fractures in 31 cases (21.38%) and four-wall fractures in 15 cases (10.35%). CONCLUSIONS: There were complex orbital fracture in maxillofacial injures, CT examination is a very important tool for diagnosis,which should be applied routinely.

Adolescent↗

PubMed2004

[Soil respiration characteristics in winter wheat field in North China Plain].

Experiments were conducted at the Yucheng Comprehensive Experimental Station of the Chinese Academy of Sciences during 2002-2003 to investigate the respiration of a pulverous sandstone soil under cultivation of winter wheat over a growth season. The effluent CO2 was collected and analyzed by the static-chamber/gas chromatography (GC) method at a frequency of once a week in spring and autumn, once two weeks in winter, twice a week for straw manure treatment, once a week for no straw manure treatment and nitrogen fertilization treatment in summer. The results indicated that diurnal variation of soil respiration rate showed a single peak in typical winter wheat farmlands in the North China Plain, and reached the highest at about 13 o'clock, and the lowest at about 4 o'clock in the early morning. In winter wheat growth season, the soil respiration rate was 31.23-606.85 mg x m(-2) x h(-1) under straw manure, 28.99-549.66 x m(-2) x h(-1) under no straw manure, 10.46-590.86 mg x m(-2) x h(-1) in N0, 16.11-349.88 mg x m(-2) x h(-1) in N100, 12.25-415.00 mg x m(-2) x h(-1) in N200, and 23.01-410.58 mg x m(-2) x h(-1) in N300, showing a similar seasonal variation tendency with soil temperature. Among all treatments, the straw manure had the most distinct soil respiration, though the soil respiration also increased slightly with increasing nitrogen fertilization. Soil respiration increased exponentially with increasing soil temperature, and the correlation of soil temperature at the depth of 5 cm was the best. This relationship was usually described with the Q10 model, which represented the sensitivity of soil respiration to temperature. Q10 was not a fixed value, which varied with the depth at which the temperature was measured and the depth of the active soil layer and soil temperature. At same time, the Q10 value decreased with increasing soil temperature. Soil water content was another important factor affecting soil respiration rate, but in this region, the relationship between soil respiration and soil moisture was poor, and no distinct rules were shown. The average net photosynthesis rate of winter wheat had a close relation with soil respiration rate. The differences between them showed that the photosynthetic uptake of CO2 was beyond emission of soil respiration during the period from return green to mature, and the winter wheat farmland was a sink of CO2.

Carbon Dioxide↗

PubMed2004

[Diurnal variation of winter wheat water and heat fluxes of a simulation with photosynthesis-evapotranspiration coupled model].

A coupled model of winter wheat photosynthesis-evapotranspiration was established based on SPAC theory. Sensible heat and latent heat fluxes were calculated by two-layer model proposed by Shuttleworth and Wallace, and photosynthesis and evapotranspiration were coupled by the parameterization of canopy resistance. The model was validated with the data measured by eddy covariance method. The results showed that the simulated and observed values were accordant, and the model could simulate the diurnal variation of sensible heat and latent heat fluxes very well. Sensitivity analysis indicated that the sensitive parameters of canopy transpiration were wilting point, stomata conductance, reflectivity of leaves to infrared radiation, and convexity of photosynthesis response to light, while the sensitive parameter of soil evaporation was soil resistance. The model could be used to study the interactions between water and heat fluxes and environmental factors, and to instruct the irrigation scheme in the field.

Energy Metabolism↗

PubMed2003

A p53-independent G1 cell cycle checkpoint induced by the suppression of protein kinase C alpha and theta isoforms.

The protein kinase C (PKC) family consists of multiple isoforms that are involved in the regulation of diverse cellular responses. Suppression of PKC induces growth arrest in various types of cells. However, the underlying molecular mechanisms have not been thoroughly investigated. In this report, we demonstrated that the concurrent inhibition, rather than separate inhibition, of phorbol ester-dependent PKC alpha and theta isoforms is crucial for the induction of G1 cell cycle arrest and that this negative cell cycle regulation is via p53-independent mechanisms. PKC suppression-mediated growth arrest is associated with the induction of cell cycle inhibitor p21WAF1/CIP1 and the occurrence of hypophosphorylated Rb. The G1 checkpoint induced by the suppression of PKC occurs not only in murine Swiss3T3 but also in p53-deficient cells and human lung cancer cells containing mutated p53. Luciferase and nuclear run-off assays demonstrated that p21WAF1/CIP1 is, in part, transcriptionally regulated in response to the suppression of PKC alpha and theta. However, the stability of p21 mRNA is also augmented after the addition of PKC alpha and theta antisense oligonucleotides, indicating the involvement of post-transcriptional mechanisms in p21WAF1/CIP1 expression. These data suggest the existence of a cell cycle checkpoint pathway regulated by PKC alpha and theta isoforms. Furthermore, our findings support the notion that G1 checkpoint control can be restored in tumor cells containing abnormal p53, by targeting the PKC-regulated p21WAF1/CIP1 induction.

3T3 Cells↗

PubMed2003

Heparan sulfates expressed in the distal lung are required for Fgf10 binding to the epithelium and for airway branching.

Fibroblast growth factor (Fgf) 10 is a critical regulator of bud formation during lung morphogenesis. fgf10 is expressed in distal lung mesenchyme at sites of prospective budding from the earliest developmental stages and signals through its epithelial receptor Fgfr2b. Experiments in intact lung organ cultures demonstrate that Fgf10 is a chemotactic factor for distal, but not for proximal, epithelium. This differential response suggests the involvement of an additional mechanism regulating Fgf10-Fgfr2b interactions, because Fgfr2b is uniformly expressed throughout the respiratory tract. Here we use an immunohistochemistry-based binding assay to show that O-sulfated heparan sulfates (HS) are critical for Fgf10 binding to the distal epithelium. We show that altering endogenous gradients of HS sulfation with sodium chlorate or over-O-sulfated synthetic heparin in lung organ cultures dramatically decreases Fgf10 binding. Moreover, we show that under these conditions epithelial binding is not improved by providing exogenous FGF10. Our data suggest that, not only ligand availability, but also the presence of specific patterns of HS modification in the distal lung epithelium are critical determinants of Fgf10 binding to the epithelium and signaling.

Animals↗

PubMed2003

Heparan sulfate-FGF10 interactions during lung morphogenesis.

Signaling by fibroblast growth factor 10 (FGF10) through FGFR2b is essential for lung development. Heparan sulfates (HS) are major modulators of growth factor binding and signaling present on cell surfaces and extracellular matrices of all tissues. Although recent studies provide evidence that HS are required for FGF-directed tracheal morphogenesis in Drosophila, little is known about the HS role in FGF10-mediated bud formation in the vertebrate lung. Here, we mapped HS expression in the early lung and we investigated how HS interactions with FGF10-FGFR2b influence lung morphogenesis. Our data show that a specific set of HS low in O-sulfates is dynamically expressed in the lung mesenchyme at the sites of prospective budding near Fgf10-expressing areas. In turn, highly sulfated HS are present in basement membranes of branching epithelial tubules. We show that disrupting endogenous gradients of HS or altering HS sulfation in embryonic lung culture systems prevents FGF10 from inducing local responses and markedly alters lung pattern formation and gene expression. Experiments with selectively sulfated heparins indicate that O-sulfated groups in HS are critical for FGF10 signaling activation in the epithelium during lung bud formation, and that the effect of FGF10 in pattern is in part determined by regional distribution of O-sulfated HS. Moreover, we describe expression of a HS 6-O-sulfotransferase preferentially at the tips of branching tubules. Our data suggest that the ability of FGF10 to induce local budding is critically influenced by developmentally regulated regional patterns of HS sulfation.

Animals↗

PubMed2003

Impact of p53 knockout and topotecan treatment on gene expression profiles in human colon carcinoma cells: a pharmacogenomic study.

To uncover transcriptional stress responses related to p53, we used cDNA microarrays (National Cancer Institute Oncochips comprising 6500 different genes) to characterize the gene expression profiles of wild-type p53 HCT-116 cells and an isogenic p53 knockout counterpart after treatment with topotecan, a specific topoisomerase I inhibitor. The use of the p53 knockout cells had the advantage over p53-overexpressing systems in that p53 activation is mediated physiologically. RNA was extracted after low (0.1 microM)- and high (1 microM)-dose topotecan at multiple time points within the first 6 h of treatment. To facilitate simultaneous study of the p53 status and pharmacological effects on gene expression, we developed a novel "cross-referenced network" experimental design and used multiple linear least squares fitting to optimize estimates of relative transcript levels in the network of experimental conditions. Approximately 10% of the transcripts were up- or down-regulated in response to topotecan in the p53+/+ cells, whereas only 1% of the transcripts changed in the p53-/- cells, indicating that p53 has a broad effect on the transcriptional response to this stress. Individual transcripts and their relationships were analyzed using clustered image maps and by a novel two-dimensional analysis/visualization, gene expression map, in which each gene expression level is represented as a function of both the genotypic/phenotypic difference (i.e., p53 status) and the treatment effect (i.e., of topotecan dose and time of exposure). Overall, drug-induced p53 activation was associated with a coherent genetic program leading to cell cycle arrest and apoptosis. We identified novel p53-induced and DNA damage-induced genes (the proapoptotic SIVA gene and a set of transforming growth factor beta-related genes). Genes induced independently of p53 included the antiapoptotic cFLIP gene and known stress genes related to the mitogen-activated protein kinase pathway and the Fos/Jun pathway. Genes that were negatively regulated by p53 included members of the antiapoptotic protein chaperone heat shock protein 70 family. Finally, among the p53-dependent genes whose expression was independent of drug treatment was S100A4, a small Ca(2+)-binding protein that has recently been implicated in p53 binding and regulation. The new experimental design and gene expression map analysis introduced here are applicable to a wide range of studies that encompass both treatment effects and genotypic or phenotypic differences.

Antineoplastic Agents↗

PubMed2003

Carotid artery and jugular vein invasion of oral-maxillofacial and neck malignant tumors: diagnostic value of computed tomography.

OBJECTIVE: This study aimed to disclose the diagnostic value of computed tomography (CT) images in detecting carotid artery and jugular vein invasion by oral-maxillofacial and neck malignant tumors. Study design Forty-three patients (44 tumors) who had had enhanced CT examination before surgical treatment of oral-maxillofacial and neck malignant tumors were evaluated. The CT manifestations of all tumors were retrospectively compared with the surgical findings. RESULTS: Surgical findings recorded that the oral-maxillofacial and neck tumors adhered to 11 of 44 common carotid arteries (CCA) or internal carotid arteries (ICA) and 25 of 44 jugular veins (JV). The abnormal CT manifestations of the 44 oral-maxillofacial and neck malignant tumors with CCA, ICA, and JV involvement consisted of 6 types: type I, compression and deformation of CCA or ICA in 4 tumors and JV in 28 tumors; type II, obliteration of IJV on segmental axial CT views in 13 tumors; type III, displacement of CCA or ICA in 14 tumors and JV in 18 tumors; type IV, tumor encasement of greater than 180 degrees of the circumference of the carotid vessels in 5 tumors; type V, the segmental deletion of fat or fascial planes between tumor and CCA or ICA in 16 tumors and JV in 33 tumors; and type VI, ill-defined CCA or ICA wall in 7 tumors. The respective sensitivity, specificity, and accuracy were 36.4%, 100%, and 84.1% for compression and deformation of CCA or ICA; 84%, 63.2%, and 75% for compression and deformation of JV; 52%, 100%, and 72.7% for obliteration of JV in segmental axial CT views; 36.4% to 52%, 53.8% to 69.7%, and 61.4% for displacement of CCA or ICA and JV; 18.5%, 100%, and 50% for tumor encasement of greater than 180 degrees of the circumference of the carotid vessels; 90.9%, 81.8%, and 84.1% for partial fat or fascia deletion between tumor and CCA or ICA; 92%, 47.4%, and 72.7% for partial fat or fascia deletion between tumor and JV; and 36.4%, 90.9%, and 77.3% for ill-defined CCA or ICA wall. CONCLUSIONS: Various CT findings are of value in the diagnosis of oral-maxillofacial and neck malignant tumors that affect the carotid arteries and jugular veins. Comparatively, the signs of compression and deformation of the CCA or ICA, segmental obliteration of the JV, undefined CCA or ICA wall, and fat or fascial plane deletion between a tumor and the CCA or ICA may be valuable in diagnosing ICA and JV invasion, although accurate diagnosis of CCA or ICA involvement by the oral-maxillofacial and neck malignant tumors remains difficult.

Adipose Tissue↗

PubMed2003

[The effects of PTEN gene on migration and FAK phosphorylation of SMMC-7721 human hepatocarcinoma cell line].

PTEN is a major tumor suppressor gene that encodes a dual-specificity phosphatase with high sequence similarity to the cytoskeletal protein tensin. PTEN may be involved in the formation and disassembly of focal adhesion and affect cell migration. In the present study, PTEN expression plasmid was constructed and transfected into the hepatoma cell line SMMC-7721 to analyze the alterations of cell motility and FAK tyrosine phosphorylation. It was observed that the overexpression of PTEN gene significantly inhibited cell motility on extracellular matrix (Fn), and the cell migration on fibronectin was reduced by 35%. Similarly, at 30-min and 60-min, the cell spreading on Fn but not on polylysine was inhibited by 29% and 26% respectively. The data obtained from immunoprecipitation and immunoblotting analyses showed that the overexpression of PTEN did not affect FAK expression but resulted in a decrease in FAK tyrosine phosphorylation. The level of FAK phosphorylation was inversely correlated with the level of PTEN protein in three cell lines. It was also found that the overexpression of PTEN led to growth inhibition, with the number of cells in S phase reduced by 16%. These results indicate that PTEN exerts its tumor-suppressive effects on hepatocellular carcinoma cells through the inhibition of cell motility and cell cycle progression.

Blotting, Western↗