RESUMEN
Side population (SP) cells are a small subset of cells isolated from a cultured cancer cell line with characteristics similar to those of cancer stem cells, such as high metastatic and tumorigenic potentials. However, the molecular mechanisms remain unclear for the malignant properties of SP cells. In this study, SP cells were isolated by staining cultured HCCLM3 cells with fluorescent DNA-binding dye Hoechst 33342 and sorted by flow cytometry. The proportion of SP cells was 2.79%±0.19% in the HCCLM3 cell line. Compared with non-SP cells, SP cells possessed stronger capability of sphere formation and tumorigenicity, and expressed higher levels of CD133 and CD90. Then, we found that SP cells possessed 25 upregulated and 34 downregulated microRNAs with differences of >3-fold. As one of the upregulated microRNAs, miR-192-5p was computationally predicted to target semaphorin 3A (SEMA3A), a potent suppressor of tumor angiogenesis in various cancer models. Luciferase reporter assay showed that SEMA3A was a direct target of miR-192-5p. Overexpression of miR-192-5p promoted cell proliferation and metastasis targeting SEMA3A in HCCLM3 cells. Immunohistochemical staining revealed that SEMA3A expression was significantly reverse associated with metastasis in hepatocellular carcinoma tissues. The results indicate that miR-192-5p contributes to targeting SEMA3A in HCCLM3 cells, and this may be used as a target in targeted therapy and a marker for cancer behavior and prognosis.
Asunto(s)
Carcinoma Hepatocelular/genética , Neoplasias Hepáticas/genética , MicroARNs/genética , Semaforina-3A/metabolismo , Carcinogénesis , Proliferación Celular , Regulación Neoplásica de la Expresión Génica , Células Hep G2 , Humanos , Inmunohistoquímica , Metástasis de la Neoplasia , Semaforina-3A/genética , Células Tumorales CultivadasRESUMEN
We have previously shown that overexpression of RASSF1A inhibits the growth of human gastric cancer SGC7901 cells, but the underlying mechanism remains unknown. In this study, the differential protein expression by RASSF1A gene in human gastric cancer cell line SGC7901 was determined by 2-D gel electrophoresis combined with matrix-assisted laser desorption/ionization-time of flight mass spectrometry (MALDI-TOF MS) and bioinformatics. Differential expression analysis of the protein profiles by RASSF1A gene identified a total of 35 protein spots, of which 10 were up-regulated and 25 were down-regulated. Eight proteins were identified by MALDI-TOF MS: Galectin-1, TRP-14, ACBP, PSMB5, PSMB4, TIM, vimentin, CD79α. RASSF1A up-regulated the mRNA expression of Galectin-1, TRP-14, ABCP in SGC7901. RASSF1A also led to an increased expression of Galectin-1 protein in SGC7901 confirmed by western blotting and immunocytochemistry analysis. RASSF1A inhibited the activity of NF-κB in SGC7901 cells. These data indicated that Galectin-1 may be playing a role in RASSF1A signaling in SGC7901.
Asunto(s)
Galectina 1/metabolismo , Regulación Neoplásica de la Expresión Génica , Neoplasias Gástricas/genética , Neoplasias Gástricas/metabolismo , Proteínas Supresoras de Tumor/genética , Western Blotting , Línea Celular Tumoral , Electroforesis en Gel Bidimensional , Galectina 1/biosíntesis , Galectina 1/genética , Humanos , ARN Neoplásico/genética , ARN Neoplásico/metabolismo , Reacción en Cadena de la Polimerasa de Transcriptasa Inversa , Transducción de Señal , Espectrometría de Masa por Láser de Matriz Asistida de Ionización Desorción , Proteínas Supresoras de Tumor/metabolismo , Regulación hacia ArribaRESUMEN
<p><b>OBJECTIVE</b>To study the effects of short hairpin RNA (shRNA) mediated gene silencing of β-catenin on the biological characteristics of esophageal carcinoma cells, and to provide theoretical and experimental evidence for the gene therapy of esophageal carcinoma through target inhibition of β-catenin gene.</p><p><b>METHODS</b>Single strand DNA was synthesized according to the hairpin RNA sequence, and then subcloned into eukaryotic expression vector pGenesil-3 to construct a shRNA-expression pDNAs driven by human U6 promoter of β-catenin (pGen-3-CTNNB1). One additional construct of random siRNA (pGen-3-con) without homologous to any human genes was constructed in a similar fashion as control.Positive clones were identified and verified by restriction cleavage and DNA sequencing analyses. pGen-3-CTNNB1 and pGen-3-con were then transfected into esophageal carcinoma cell line Eca-109 with liposome, respectively. Positive colonies were selected with G418. Expression of β-catenin protein and mRNA in the transfected and nontransfected Eca-109 cells were examined by Western blotting, immunofluorescence and RT-PCR, respectively. Xenograft tumor model was used to compare the tumorigenesis of three different cells.Expressions of β-catenin in all tumor tissues were examined by immunohistochemistry staining. The invasive abilities of three different cells were examined with transwell invasion filter and Matrigel.</p><p><b>RESULTS</b>β-catenin expression levels were found markedly decreased in Eca-109 cells transfected with pGen-3-CTNNB1. In vivo, transfection with β-catenin shRNA greatly impeded the tumor growth, pGen-3-con (1.18 ± 0.13) g, Eca-109 (1.38 ± 0.21) g, pGen-3-CTNNB1 (0.42 ± 0.09) g, P < 0.05. Immunohistochemistry staining showed a significantly decreased expression of β-catenin in β-catenin shRNA transfected cells than in random shRNA transfected and nontransfected cells (P < 0.05). The infiltration abilities of esophageal carcinoma cells were significantly suppressed, pGen-3-con (81 ± 5)/HPF, Eca-109 (77 ± 6)/HPF, pGen-3-CTNNB1 (41 ± 4)/HPF, P < 0.01; along with significantly decreased migration abilities, pGen-3-con (73 ± 5)/HPF, Eca-109 (69 ± 5)/HPF, pGen-3-CTNNB1 (38 ± 4)/HPF (P < 0.05).</p><p><b>CONCLUSIONS</b>There are abnormal expression of β-catenin and activation of Wnt signaling pathway in human esophageal carcinoma cell line Eca-109. RNA interference targeting β-catenin gene suppresses the growth of xenograft tumorigenesis in nude mouse and the invasiveness and metastatic capability of esophageal carcinoma cells.</p>
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Animales , Femenino , Humanos , Ratones , Carcinoma de Células Escamosas , Genética , Metabolismo , Patología , Línea Celular Tumoral , Movimiento Celular , Neoplasias Esofágicas , Genética , Metabolismo , Patología , Silenciador del Gen , Vectores Genéticos , Ratones Endogámicos BALB C , Ratones Desnudos , Invasividad Neoplásica , Trasplante de Neoplasias , Plásmidos , ARN Mensajero , Metabolismo , ARN Interferente Pequeño , Genética , Distribución Aleatoria , Transducción de Señal , Transfección , Carga Tumoral , Proteínas Wnt , Metabolismo , beta Catenina , Genética , Metabolismo , FisiologíaRESUMEN
OBJECTIVE@#To analyze the causes of medical malpractice in patients with tumor, to determine the medical responsibility, and to recommend the related preventions.@*METHODS@#Seventy four medical malpractice cases, which were involved in tumor and collected from 2000 to 2009 in medicolegal expertise center of west China, were analyzed retrospectively.@*RESULTS@#The medical malpractice cases in the patients with tumor showed an increasing tendency in recent years. The main causes are missed diagnosis, misdiagnosis, improper chemotherapy and neglect of complications. The causes of medical malpractice were different in the different levels of medical services. The occurrence of medical malpractice in surgery and OB-GYN showed more frequent than the others.@*CONCLUSION@#Forensic pathology autopsy is important to resolve medical malpractice of tumor patients by finding out the cause of death and clarifying the medical responsibility. The occurrence of medical malpractice could be reduced by the clinical doctors through improving serve consciousness, obtaining the patients' trust, improving the medical treatment, following related laws and rules, fulfiling duty of medical careness.
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Adulto , Femenino , Humanos , Masculino , Persona de Mediana Edad , Distribución por Edad , Testimonio de Experto , Patologia Forense , Administración Hospitalaria , Responsabilidad Legal , Mala Praxis/estadística & datos numéricos , Errores Médicos/estadística & datos numéricos , Neoplasias/terapia , Estudios Retrospectivos , Distribución por SexoRESUMEN
OBJECTIVE@#To explore mitochondrial DNA (mtDNA) extraction effects of different parts from sarcosaphagous insects using improved cetyltriethylammnonium bromide (CTAB) method.@*METHODS@#Thirteen Lucilia sericata (Meigen) and 13 Nicrophorus fossor (Erichson) were collected from the corpses of rabbits placed on the outdoor lawn in Huhehot district. Four parts (head, chest muscle, legs and wings) of insect were collected, and the mtDNA of all samples were extracted using CTAB method. The purity and concentration were tested using protein and nucleic acid spectrophotometry. The integrity of the extracted mtDNA and PCR products were checked by agarose gel electrophoresis. The PCR products were sequenced and the obtained sequences were imputed into GenBank for comparison.@*RESULTS@#mtDNA were successfully extracted from 10 head samples, 6 legs samples, 4 wing samples and 13 chest muscle samples of the Lucilia sericata (Meigen). Also, mtDNA were successfully extracted from 5 head samples, 8 legs samples, 3 wing samples and 13 chest muscle samples of the Nicrophorus fossor (Erichson).@*CONCLUSION@#mtDNA can be obtained from chest muscle and other parts of sarcosaphagous insects using the improved CTAB method.
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Animales , Conejos , Escarabajos/genética , ADN Mitocondrial/aislamiento & purificación , Dípteros/genética , Complejo IV de Transporte de Electrones/genética , Electroforesis en Gel de Agar , Entomología , Medicina Legal/métodos , Reacción en Cadena de la Polimerasa/métodos , Análisis de Secuencia de ADN , Especificidad de la EspecieRESUMEN
Estimation of postmortem interval (PMI) is one of the problems that need to be solved for forensic examination of the dead body. Accurate estimation of PMI has great values to criminal investigation and trial. The levels of chemical components in human vitreous humor are changed with time after death, which can help estimate the PMI. The levels of certain chemical components, such as potassium, magnesium, ammonia, urea, creatinine, uric acid, hypoxanthine, lactic acid and so on, in human vitreous humor will gradually increase with time after death, while others such as calcium, sodium, enzymes, glucose, vitamin C and so on will decrease. The updates and advances in those studies were reviewed in this article.
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Humanos , Calcio/análisis , Patologia Forense , Magnesio/análisis , Cambios Post Mortem , Potasio/análisis , Sodio/análisis , Factores de Tiempo , Cuerpo Vítreo/químicaRESUMEN
<p><b>OBJECTIVE</b>To study the role of activator protein-1 (AP-1) in the up-regulation expression of tumor necrosis factor-alpha (TNF-alpha) and transforming growth factor-beta1(TGF-beta(1)) in silica-stimulated macrophage cells (RAW264.7).</p><p><b>METHODS</b>RAW264.7 cells were treated with AP-1 inhibitor Curcumin. The expression of c-jun and c-fos in nuclear protein was detected by western blotting. The level of TNF-alpha and TGF-beta(1) protein in the cell supernatant was measured using enzyme-linked immunoadsorbent assay (ELISA). Meanwhile the expression of TNF-alpha and TGF-beta(1) mRNA was also monitored by reverse transcriptase-polymerase chain reaction (RT-PCR).</p><p><b>RESULTS</b>The nucleoprotein expression of c-jun and c-fos in 10 and 20 micromol/L Curcumin prevention group (1.150 +/- 0.020, 1.010 +/- 0.108, 80.430 +/- 0.023, 0.256 +/- 0.015) were lower than those in silica-stimulated group (1.550 +/- 0.029, 0.860 +/- 0.036) (P < 0.01). In 20 micromol/L Curcumin prevention group and silica stimulated group, the expression of TNF-alpha protein were 23.58 +/- 45.78 and 32.12 +/- 5.34, and the expression of TGF-beta(1) protein were 1582.18 +/- 437.52 and 55.60 +/- 5.51 (P < 0.05 =; the expression of TNF-alpha, TGF-beta(1) mRNA were 0.74 +/- 0.01, 0.22 +/- 0.04 and 2.27 +/- 0.33, 2.96 +/- 0.15 (P < 0.05 =.</p><p><b>CONCLUSION</b>The expression of TNF-alpha, TGF-beta(1) mRNA and proteins is associated with activation of AP-1 in silica-stimulated macrophage cells.</p>
Asunto(s)
Animales , Ratones , Línea Celular , Curcumina , Farmacología , Macrófagos , Metabolismo , Proteínas Proto-Oncogénicas c-fos , Metabolismo , Proteínas Proto-Oncogénicas c-jun , Metabolismo , ARN Mensajero , Genética , Dióxido de Silicio , Farmacología , Factor de Transcripción AP-1 , Metabolismo , Factor de Crecimiento Transformador beta1 , Metabolismo , Factor de Necrosis Tumoral alfa , MetabolismoRESUMEN
OBJECTIVE@#To investigate the effect of basic fibroblast growth factor (FGF-2)on survivin and subcellular location of Smac in human small cell lung cancer (SCLC) cell NCI-H446.@*METHODS@#Western blot was used to detect the expression of survivin protein induced by FGF-2. The release of Smac from mitochondria to cytoplasm affected by FGF-2 was observed by Western blot and immunofluorescence. Apoptosis of NCI-H446 cells was detected with flow cytometry and Hoechst 33258 staining.@*RESULTS@#The expression of survivin could be up-regulated in response to FGF-2 treatment in NCI-H446 cells, and the level of survivin expression is related to the concentration and time of FGF-2 treatment. FGF-2 could inhibit the release of Smac from the mitochondria to cytoplasm induced by serum starving. FGF-2 could inhibit the apoptosis induced by serum starving.@*CONCLUSION@#FGF-2 up-regulates the expression of survivin protein in NCI-H446 cells, and blocks the release of Smac from mitochondria cytoplasm. Survivin and Smac might play important roles in the apoptosis inhibited by FGF-2.
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Humanos , Apoptosis , Proteínas Reguladoras de la Apoptosis , Citoplasma , Metabolismo , Factor 2 de Crecimiento de Fibroblastos , Farmacología , Proteínas Inhibidoras de la Apoptosis , Péptidos y Proteínas de Señalización Intracelular , Metabolismo , Neoplasias Pulmonares , Metabolismo , Patología , Proteínas Asociadas a Microtúbulos , Mitocondrias , Metabolismo , Proteínas Mitocondriales , Metabolismo , Carcinoma Pulmonar de Células Pequeñas , Metabolismo , Patología , Survivin , Células Tumorales CultivadasRESUMEN
OBJECTIVE@#To explore the effect of Twist gene on the migration and invasion of human gastric carcinoma cells.@*METHODS@#MKN28 cells, a human gastric carcinoma cell line, were transfected with PcDNA3.1-Twist plasmid by lipofectamine transfecting technique. The transfected cells were selected with geneticin. Expressions of Twist,ecadherin and vimentin protein were detected by Western blot in cells transfected Twist gene. Matrigel invision chambers were performed to analyse the cell migration and invasion.@*RESULTS@#MKN28 cells transfected with PcDNA3.1-Twist plasmid showed stronger intracellular expression of Twist protein than MKN28 cells transfected with PcDNA3.1 and MKN28 cells without transfection. The expression of ecadherin protein in MKN28 cells transfected with PcDNA3.1-Twist plasmid was significantly decreased compared with that in MKN28 cells transfected with PcDNA3.1 and MKN28 cells without the transfection. However, The expression of vimentin protein in MKN28 cells transfected with PcDNA3.1-Twist plasmid was significantly increased compared with that in MKN28 cells transfected with PcDNA3.1 and MKN28 cells without transfection. The migration and invasion ability of Twist+ - MKN28 cells were stronger than that of MKN28 cells transfected with PcDNA3.1 and MKN28 cells without transfection.@*CONCLUSION@#Twist gene may promote the migration and invasion ability of gastric carcinoma cells through epithelial mesenchymal transition.
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Humanos , Cadherinas , Movimiento Celular , Genética , Invasividad Neoplásica , Metástasis de la Neoplasia , Neoplasias Gástricas , Genética , Metabolismo , Patología , Transfección , Células Tumorales Cultivadas , Proteína 1 Relacionada con Twist , Genética , VimentinaRESUMEN
<p><b>OBJECTIVE</b>To study the role of PTEN gene involved in the biological behavior of human gastric carcinoma cells and underlying molecular mechanisms.</p><p><b>METHODS</b>Gastric carcinoma cell line, SGC7901, was transfected with plasmid PBP-PTEN and stable high PTEN expression clones were selected by Western blot and cell immunohistochemistry screening. Cell proliferation rate and apoptosis index of transfected cells were investigated by growth curve analysis, colony-formation assay and flow cytometry (FCM). Expressions of vascular endothelial growth factor (VEGF), matrix metalloprotease-2 (MMP-2) and MMP-9 proteins in cell culture supernatant and cytoplasm were determined by ELISA, gelatin zymogram, Western blot and cell immunohistochemistry.</p><p><b>RESULTS</b>Stable clone with high level expression of PTEN was successfully established (PTEN-SGC7901). Cell doubling time of PTEN-SGC7901 was longer than that of the control cells (P < 0.05). The size and colony-forming efficiency of PTEN-SGC7901 cells deceased compared with those of the control. The relative colony-inhibition efficiency of PTEN-SGC7901 to SGC7901 (naïve untransfected) and PBP-SGC7901 (control vector transfected) cells were 69.8% and 64.8%, respectively. PTEN-SGC7901 clone had more cells at G1 phase (P < 0.05) compared with that of the control. However, the apoptosis index did not show significant differences among the three groups (P > 0.05). There were significantly less VEGF and MMP-9 protein expressions in the PTEN-SGC7901 culture supernatant and cytoplasm (P < 0.05). In contrast, the MMP-2 expression among three cell groups had no significant difference (P > 0.05).</p><p><b>CONCLUSIONS</b>PTEN expression suppresses the growth and proliferation of gastric carcinoma cell SGC7901, possibly through an inhibition of the expressions of VEGF and MMP-9.</p>
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Humanos , Apoptosis , Ciclo Celular , Línea Celular Tumoral , Proliferación Celular , Regulación Neoplásica de la Expresión Génica , Metaloproteinasa 2 de la Matriz , Metabolismo , Metaloproteinasa 9 de la Matriz , Metabolismo , Fosfohidrolasa PTEN , Genética , Metabolismo , Plásmidos , Neoplasias Gástricas , Metabolismo , Patología , Transfección , Factor A de Crecimiento Endotelial Vascular , MetabolismoRESUMEN
<p><b>OBJECTIVE</b>To investigate the effects of SiO(2) on the expression of alpha-smooth muscle actin (alpha-SMA) in human lung fibroblasts in vitro and vivo.</p><p><b>METHODS</b>The experimental group comprised 32 rats while 32 rats were included in the control. In vivo, the expression of alpha-SMA in lung tissues of rats exposed to SiO(2), the supernate of RAW264.7 cells, SiO(2) and the growth factor beta(1) (TGF-beta(1)) were investigated, respectively.</p><p><b>RESULTS</b>(1) alpha-SMA positive myofibroblasts appeared in the lung tissues of the 28th day groups exposed to SiO(2). (2) The expression of alpha-SMA in HLF-02 cells was unregulated by TGF-beta(1) and supernate of RAW264.7 cells exposed to SiO(2). (3) The expression of alpha-SMA in HLF-02 cells was not induced by SiO(2).</p><p><b>CONCLUSION</b>Myofibroblasts related to silicosis, and the appearance of myofibroblasts (in vitro) are independent on direct stimulation by SiO(2), but related to the mediator (TGF-beta(1)) secreted by SiO(2) stimulated macrophages.</p>
Asunto(s)
Animales , Ratas , Actinas , Genética , Células Cultivadas , Fibroblastos , Metabolismo , Pulmón , Biología Celular , Metabolismo , Macrófagos Peritoneales , Ratas Sprague-Dawley , Dióxido de Silicio , Farmacología , Silicosis , Metabolismo , Patología , Factor de Crecimiento Transformador beta1 , FarmacologíaRESUMEN
<p><b>OBJECTIVE</b>To study the expression and localization of nuclear transcription factor Sp1 in macrophages after stimulated by silicon dioxide in vivo and in vitro.</p><p><b>METHODS</b>Forty Sprague Dawley rats were randomly divided into the control group and the silica exposure group, 20 in each group. The rat silicosis models were established by direct tracheal instillation of silica into rat lung (0.2 g/kg) only once while the control group was instilled with equal amount of saline. Animals were killed at 1st, 7th, 14th, 21st and 28th day after instillation. Dynamic changes of Sp1 protein expression and its cellular localization were detected by immunohistochemistry in pulmonary macrophages. In vitro, Sp1 mRNA and protein expression and their dynamic changes were monitored by RT-PCR and western blotting after stimulated by silicon dioxide in cultured RAW264.7 macrophages respectively. Cellular localization of Sp1 protein was characterized by immunocytochemistry.</p><p><b>RESULTS</b>Compared to the control group, the Sp1 protein expression was increased in pulmonary macrophages and reached the peak at the 14th day in the silica exposure group. In vitro, the Sp1 mRNA level began to rise at 30 minutes after the administration of silicon dioxide and reached the peak at 240 minutes and then decreased to the minimal level at 960 minutes. The Sp1 total protein and nuclear protein also exhibited the similar trend. The former reached the peak at 240 minutes and the latter at 480 minutes. The significant nuclear translocation of Sp1 protein was observed at 120 minutes after the administration of silicon dioxide and became most significant at 480 minutes.</p><p><b>CONCLUSION</b>Silicon dioxide can activate nuclear transcription factor Sp1 in macrophages in vivo and in vitro. Sp1 might play an important pathogenic role in the development of silicosis.</p>
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Animales , Masculino , Ratas , Células Cultivadas , Regulación de la Expresión Génica , Inmunohistoquímica , Macrófagos Alveolares , Metabolismo , Macrófagos Peritoneales , Metabolismo , ARN Mensajero , Genética , Distribución Aleatoria , Ratas Sprague-Dawley , Reacción en Cadena de la Polimerasa de Transcriptasa Inversa , Dióxido de Silicio , Farmacología , Factor de Transcripción Sp1 , GenéticaRESUMEN
OBJECTIVE@#To detect the expressions of TG-interacting factor (TGIF), matrix metalloproteinase 9 (MMP9) and vascular endothelial growth factor (VEGF) proteins, and to analyze their clinicopathological relationship in gastric cancer.@*METHODS@#Vascular invasion and remote metastasis were examined in nude mice inoculated with SGC-7901 cells, vector control cells or TGIF transfected cells via serial sections, and sequentially the expressions of MMP2, MMP9 and VEGF proteins in tumor tissues from nude mice were detected by immunohistochemical staining. At the same time, TGIF, MMP9 and VEGF proteins were examined in 76 patients with gastric carcinoma, and the relationships between the expressions of the three proteins and clinicopathological features were analyzed.@*RESULTS@#Metastasis was not observed in nude mice inoculated with any cells. There were cancerous embolisms in nude mice tumor tissue inoculated with SGC-7901 cells and vector control cells, but not in TGIF transfected cells. The expressions of MMP9 and VEGF proteins were higher in the tumor tissues originated from SGC-7901 cells and vector control cells than that from TGIF transfected cells. The expression of MMP2 had no distinct difference among the tumor tissues originated from the three cells. The positive rate of TGIF protein in gastric carcinoma was 46.1% (35/76), obviously lower than that in surgical marginal mucosa (78.1%) (P < 0.05). Low expression of TGIF protein correlated significantly with the metastasis of lymph node. The positive rates of MMP9 and VEGF proteins in gastric carcinoma were 59.2% and 56.6%, respectively, obviously higher than that in surgical marginal mucosa (31.3%) (P < 0.05). High expressions of both MMP9 and VEGF also correlated significantly with the metastasis of lymph node. The expression level of VEGF protein was also associated with the invasion of gastric carcinoma (P < 0.05). The expression of TGIF protein reversely correlated with that of MMP9 and VEGF proteins (P < 0.05).@*CONCLUSION@#TGIF may inhibit the invasion and metastasis of gastric carcinoma via the downregulation of MMP9 and VEGF proteins.
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Adulto , Anciano , Animales , Femenino , Humanos , Masculino , Ratones , Persona de Mediana Edad , Proteínas de Homeodominio , Genética , Metaloproteinasa 9 de la Matriz , Genética , Ratones Endogámicos BALB C , Ratones Desnudos , Invasividad Neoplásica , Metástasis de la Neoplasia , Trasplante de Neoplasias , Distribución Aleatoria , Proteínas Represoras , Genética , Neoplasias Gástricas , Metabolismo , Patología , Factor A de Crecimiento Endotelial Vascular , GenéticaRESUMEN
OBJECTIVE@#To explore the relationship between the expressions of PTEN and the metastasis of the gallbladder cancer.@*METHODS@#The expression of PTEN and nm23 were detected by immunohistochemical staining in 32 cases of gallbladder cancer with metastasis and the staining intensity was scored semi-quantitatively, compared with the cases without metastasis.@*RESULTS@#The intensity score of PTEN and nm23 in gallbladder cancer with metastasis was 8.9947+/-4.5590 and 10.2003+/-3.9031, respectively, which was lower than that in those without metastasis (12.9433+/-4.7618 and 15.8436+/-5.6917 respectively, P < 0.01 ). The expression of PTEN was correlative with that of nm23 ( Pearson = 0.370, P < 0.05).@*CONCLUSION@#The lower expressions of PTEN and nm23 are related to the metastasis of gallbladder cancer.
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Femenino , Humanos , Masculino , Neoplasias de la Vesícula Biliar , Metabolismo , Neoplasias Hepáticas , Metabolismo , Metástasis Linfática , Nucleósido Difosfato Quinasas NM23 , Nucleósido-Difosfato Quinasa , Genética , Fosfohidrolasa PTEN , Genética , Proteínas Supresoras de Tumor , GenéticaRESUMEN
<p><b>OBJECTIVE</b>To study the effect of DPC4 gene expression on the growth of colon cancer cells and its mechanism.</p><p><b>METHODS</b>Expression plasmid pcDNA3.1-DPC4 was constructed and transfected into the colon cancer cell line SW620 by use of lipofectamine gene transfer technique. DPC4 protein expression was detected by Western blot and immunocytochemistry. The effect of DPC4 gene on the growth of SW620 cells was monitored by population doubling time (PDT) and cloning efficiency. The influence of DPC4 expression on p21WAF1 transcription was investigated by RT-PCR to detect p21WAF1 mRNA.</p><p><b>RESULTS</b>Successful expression of DPC4 protein was detected in the transfected SW620 cells. Compared with the control cells, PDT (74 h) of the DPC4 expressing cells was prolonged and the cloning efficiency (21%) decreased. In addition, the mRNA level of p21(WAF1) in DPC4 transfected cells was increased.</p><p><b>CONCLUSIONS</b>Overexpression of DPC4 gene inhibits the growth of colon cancer in vitro, and induction of p21(WAF1) expression may be an important functional aspect of DPC4.</p>