Objective To detect the tissue factor (TF) mRNA expression in hepatocellular carcinoma and to elucidate its significance. Methods TF mRNA was detected by reverse transcription-polymerase chain reaction （RT-PCR） in 27 cases of human hepatocellular carcinoma tissue specimen with their adjacent tissues and in 27 non-tumorous process tissues. Then the relationship between mRNA expression and pathological data were analyzed. Results The expression and the relative expression intensity of TF in hepatocellular carcinoma tissues were 62.96%（17/27） and 0.567±0.268 respectively, which were significantly higher than those in their adjacent tissues 〔33.33%(9/27), 0.469±0.184〕 and in 27 non-tumorous process tissue 〔29.63%(8/27), 0.353±0.121〕, Plt;0.05. The relative expression intensity of TF were associated with tumor size, intrahepatic and extrahepatic metastasis and portal vein invasion, but unrelated to gender, AFP level, differentiation, HBsAg, cirrhosis, number of tumor lesions, and lymph node metastasis (Pgt;0.05). Conclusion Expression of TF mRNA were significantly higher in hepatocellular carcinoma and in the invasive and metastatic tissue, which indicated that TF may play an important role in carcinogenesis, invasion and metastasis of hepatocellular carcinoma.
ObjectiveTo investigate the expressions of Snail and VEGF gene in invasion ductal carcinoma tissues and analyze their clinicopathologic relationship. MethodsThe expressions of Snail and VEGF gene were detected on mammary gland hyperplasia (30 cases), intraductal breast cancer (30 cases), and invasion ductal carcinoma (70 cases) by in situ hybridization， to compare with the expression difference of the two genes in the different pathological changed tissues of mammary gland and among the clinicopathological facters of invasion ductal carcinoma as well as the relationship. ResultsThe expression rate of Snai mRNA in mammary gland hyperplasia， intraductal breast cancer, and invasion ductal carcinoma was 23.3% (7/30)， 46.7% (14/30), and 81.4% (57/70), respectively, there was statistical difference among them (χ 2=32.4, Plt;0.05)； The expression rate of VEGF mRNA in mammary gland hyperplasia， intraductal breast cancer, and invasion ductal carcinoma was 33.3% (10/30)， 50.0% (15/30), and 71.4% (50/70), respectively, there was statistical difference among them (χ 2=13.4, Plt;0.05). The expression rates of Snail mRNA and VEGF mRNA in lymphatic metatasis group were significantly higher than those in no lymphatic metatasis group 〔92.7% (38/41) vs. 65.5% (19/29)， χ 2=8.29, Plt;0.05； 85.4% (35/41) vs. 51.7% (15/29), χ 2=9.42, Plt;0.05， respectively 〕. The expression rates of Snail mRNA and VEGF mRNA in Ⅲ-Ⅳ stage of TNM clinical stage were significantly higher than those in Ⅰ-Ⅱ stage 〔939% (46/49) vs. 52.4% (11/21), χ 2=14.14， Plt;0.05； 81.6% (40/49) vs. 47.6% (10/21), χ 2=8.32， Plt;0.05〕. The expressions of Snail mRNA and VEGF mRNA were related to the expressions of ER, PR, HER-2, and vessel cancer embolus （Plt;0.01）. The expressions of Snail mRNA and VEGF mRNA were not related to age, tumor size, and histological grade (Pgt;0.05). There was a positive correlation between the expressions of Snail mRNA and VEGF mRNA （r=0.67， Plt;0.05）. ConclusionsThe overexpressions of Snail mRNA and VEGF mRNA in invasion ductal carcinoma has a synergetic effect on occurrence and development, therefore, combined detecting the expressions of Snail mRNA and VEGF mRNA are some significance to predict infiltration and metastasis of the invasion ductal carcinoma.
ObjectiveTo explore the influence mechanism of proliferation and invasion in colon cancer cell after silence of phosphatase and tensin homolog deleted on chromosome 10 (PTEN) gene. MethodsRT-PCR or Western blot method was used to detect the expression of PTEN mRNA or protein among four colon cancer cell lines (HT-29, WiDr, CaCo-2, and Colo320 cell lines). small interfering RNA (siRNA) was used to synthetize PTEN siRNA and transfect it into colon cancer cells. The expression of PTEN protein after transfecting was detected by Western blot. WsT-1 and invasion assay were used to examine the effects of PTEN siRNA silence on proliferation and invasion in colon cancer cells. ResultsPTEN mRNA and protein were expressed in all the four colon cancer cell lines. After PTEN siRNA transfected into the colon cancer cells, the expressions of PTEN proteins were inhibited in all the four colon cancer cell lines (P < 0.01), and the proliferation and invasion of colon cancer cells were enhanced significantly (P < 0.01). ConclusionsPTEN siRNA play an important role in metastasis process of colon cancer via enhanced its proliferation and invasion. Therefore, the understanding biologic mechanisms for regulation of PTEN might enable better molecular target therapy of treating the colon cancer patients with metastasis.
ObjectiveTo study the expression of matrilysin in gastric cancer and to evaluate the correlation between its expression and invasion, metastasis, and prognosis. MethodsA total of 52 patients with gastric cancer were selected and followed up. The expressions of matrilysin in gastric primary focus, normal gastric mucosa, and metastatic lymph nodes were examined by reverse transcriptionpolymerase chain reaction (RT-PCR), Western blot, and immunohistochemistry, respectively. The correlations between matrilysin expression and tumor invasion, metastasis, and prognosis were assessed. ResultsThe expressions of matrilysin in gastric primary focus and metastatic lymph nodes significantly increased, while decreased or loss in normal gastric mucosa (Plt;0.001). The higher concordance was seen between the levels of mRNA and protein (Plt;0.001). Among patients with infiltrating type, penetrated serosa, area of serosa involved more than 20 cm2, and metastatic lymph nodes more than 7, the expression of matrilysin was significantly higher (Plt;0.01). The survival rate of patients with matrilysin higher expression (34.1%) was significantly lower than that with matrilysin lower expression (55.6%), χ2=9.778， P=0.002. Conclusions Up-regulated expression of matrilysin plays an important role in tumor invasion, metastasis, and poor prognosis, and it is a good molecular marker to reflect the biological behaviors of gastric cancer.
Objective To summarize the clinical features, predisposing factors, diagnosis, therapeutic outcome, and prognosis of invasive pulmonary fungal infection( IPFI) . Methods 90 cases with pathologically proved IPFI, admitted in non-intensive care unit in Xiangya Hospital from January 2005 to February 2012, were retrospectively analyzed. Results The pathogenic examination revealed Aspergillosis in 56 cases( 62. 2% ) , Cryptococcus in 18 cases( 20. 0% ) , Mucormycosis in 6 cases( 6. 7% ) , and Histoplasma in 6 cases( 6. 7% ) , etc. The underlying diseases were reported in 87 cases, and mainly included COPD, pulmonary tuberculosis, and diabetes mellitus. Cough and expectoration were the common clinical symptoms. 49 patients ( 54. 4% ) received long-term and broad-spectrum antibiotic therapy. The CT results revealed masses type in 25 cases( 27. 8%) , nodule lesions type in 15 cases( 16. 7% ) , lung consolidation type in 22 cases( 24. 4% ) , cavity type in 22 cases( 24. 4% ) , aspergilloma type in 6 cases( 6. 7% ) . 47 patients were clinical diagnosed with IPFI before biopsy with preliminary diagnosis accordance rate of 52. 2% . 31 cases ( 34. 4% ) underwent surgical resection of pulmonary lesions, and no recurrence was detected over two-year follow up. 56 cases ( 62. 2% ) received systemic anti-fugal therapy, and 43 cases( 76. 8% ) were cured or significantly improved. 3 cases ( 3. 3% ) refused any therapy. Conclusions The most frequently isolated pathogen of IPFI is Aspergillosis. The mainly underlying diseases are COPD, pulmonary tuberculosis, and diabetes mellitus. Long-termand broad-spectrum antibiotic therapy may be the major risk factor. Pathological examination is needed for final diagnosis. Surgical procedure can achieve optimal prognosis.
ObjectiveTo study the relationship between mesenchymal transition epithelial (EMT) and the occurrence, development, invasion, and metastasis of gastric cancer, and to seek to block the EMT process so as to achieve the purpose of treating tumor. MethodsThe literatures of EMT, signal pathway, and gastric cancer were analyzed by querying the PubMed. ResultsThe function and regulation mechanism of EMT is closely related to the development of gastric cancer, in the growth and proliferation of gastric cancer, tumor invasion and metastasis through a variety of signaling pathways play a role, with a great clinical application prospects. ConclusionsEMT and tumor metastasis is very close, almost involved in every process of metastasis. It is necessary to further study the relationship between EMT and cancer, including gastric carcinoma metastasis. A new way for the treatment of human gastric cancer.
【 Abstract 】 Objective Overexpressions of epidermal growth factor (EGF) and EGF receptor have been associated with progression and invasive phenotype of pancreatic cancer. However, the underlying molecular mechanism by which EGF worked in pancreatic cancer cells has not been completely understood. In this study, effect of EGF on the invasion and metastasis of pancreatic cancer cells and its regulatory mechanism were investigated. Methods The effects of EGF on the proliferation, adhesion and invasion of pancreatic cancer cells were detected by WST-1 proliferation assay, adhesion assay and invasive assay, respectively. The activity and expression of MMP-2 and MMP-9 were examined by zymography, Western blot and RT-PCR, respectively. The activity of NF- κ B was examined by EMSA. Results EGF could significantly promote the invasiveness of pancreatic cancer cells but did not affect cell proliferation or adhesion. The expressions of NF- κ B and MMP-9 were significantly increased by EGF, but EGF did not affect the activity and expression of MMP-2. Furthermore, EGF stimulated the NF- κ B binding activity. Pretreatment with NF- κ B inhibitors, pyrrolidine dithiocarbamate (PDTC), could significantly inhibit the activity of NF- κ B induced by EGF. Meanwhile, the EGF-induced expression and activity of MMP-9, as well as cell invasiveness were also inhibited by NF- κ B inhibitor. Conclusion EGF could increase the expression and promote the invasiveness of MMP-9 via the activation of NF- κ B in pancreatic cancer cells, which implies that NF- κ B inhibitant, such as PDTC, may diminish the invasiveness of pancreatic cancer cells.
ObjectiveTo investigate the expression of β-catenin and Galectin-3 protein in human cervical carcinoma and its clinical pathological significance. MethodsEighty-three cervical specimens were collected from January 2010 to June 2013. By immunohistochemical method, β-catenin and Galectin-3 expression of the 83 cases of cervical carcinoma, 45 cases of intraepithelial neoplasia (CIN) and 25 normal cervix tissue (control) were detected. ResultsThe positive expression rate in cervical carcinoma of β-catenin and Galectin-3 was respectively 74.70% and 81.93%, which was significantly higher than that in intraepithelial neoplasia (ⅠandⅡ) and normal cervical tissue (P<0.05). Compared with cervical cancer, the expression of β-catenin and Galectin-3 in CINⅢ had no statistical significance (P>0.05). The positive expression of β-catenin was significantly correlated with histological grade of cervical cancer tissue, International Federation of Gynecology and Obstetrics grade and lymph node metastasis (P<0.05). The positive expression of Galectin-3 was closely related to histological grade of cervical cancer tissue and lymph node metastasis (P>0.05). Both β-catenin and Galectin-3 expression had no relationship with other clinical pathological parameters, such as age of patients, tumor size and pathological pattern of tumor (P>0.05). β-catenin expression had significant positive correlation with that of Galectin-3 (r=0.327, P=0.002). ConclusionThe expression of Galectin-3 and β-catenin increases obviously and is associated with abnormal clinical parameters (invasion or metastasis) in patients with cervical cancer. Galectin-3 and β-catenin may act as cancer metastasis and prognostic indicators in these patients.
ObjectiveTo investigate the influence of EZH2 gene down-regulation by RNA interference on the proliferation and invasion of human glioma cell line U251. MethodsThe recombinant plasmid of small hairpin RNA targeting EZH2 gene was constructed, and transfected into gioma U251 cells by electroporation. The expression of EZH2 mRNA and protein in the cells was detected by using reverse transcriptase-polymerase chain reaction and Western blot respectively; the viability of cells was determined by using methyl thiazol tetrazo1ium assay; and the invasiveness of U251 cells was tested by Transwell cabin. ResultsThe expression levels of EZH2 mRNA in U251 cells were detected in a significantly lower proportion in the EZH2-shRNA group (0.19±0.02) than that in the untransfected group (1.13±0.05) and the control-shRNA-GFP group (1.15±0.05). The expression levels of EZH2 protein in U251 cells were detected in a significantly lower proportion in the EZH2-shRNA group (0.20±0.02) than that in the untransfected group (1.03±0.03) and the control-shRNA-GFP group (0.97±0.06). The proliferation rates in EZH2-shRNA group were significantly decreased as compared with those in the untransfected group and control-shRNA-GFP group (24 hours after transfection:60.13%±3.15%, 100.00%±9.31%, 100.03%±9.35%; 48 hours after transfection:53.01%±3.14%, 100.00%±9.13%, 99.58%±9.27%; P<0.05) and Transwell cabin suggested that the invasiveness of U251 cells was significantly decreased (46.00±2.82, 60.67±5.71, 61.00±2.48; P<0.01). ConclusionEZH2-targeted RNA interference can reduce the proliferation and invasion of human glioma cells, which suggests that EZH2 shRNA may be a potential gene therapeutic target of human glioma.
ObjectiveTo investigate effect of small interfering RNA (siRNA) targeting inhibition of growth hormone receptor (GHR) on proliferation and invasion of human liver cancer line SMMC-7721. MethodsSMMC-7721 cells were transfected with siRNA targeting human GHR by GenMuteTM transfection regent.The cells were divided into three groups:blank control group (non-transfected siRNA),negative control group (transfected with non-specific siRNA),and specificity transfected group (transfected with expression specifically interfere by GHR siRNA).the relative expression of GHR mRNA was detected by using real-time PCR.the expression of GHR protein was detected by using Western blot.The cell proliferation was assessed by CCK-8 assay.And the ability of invasion was examined by Transwell assay. ResultsThe expressions of GHR mRNA and GHR protein in the specificity transfected group were significantly lower than those in the blank control group (P<0.05) and the negative control group (P<0.05).Compared with the blank control group and the negative control group,the absorbance value and the number of migrating cells of SMMC-7721 cells were decreased obviously (P<0.05) in the specificity transfected group. ConclusionsiRNA targeting human GHR could reduce capability of proliferation migration and invasion of SMMC-7721 cells.