An in vitro study of the relationship between KiSS-1 expression and hepatoma carcinoma cell proliferation, adhesion, and invasion / 中华肝脏病杂志

<p><b>OBJECTIVE</b>To investigate the impact of expression of kisspeptin-1 (KiSS-1) metastasis-suppressor gene on the proliferative, adhesive and invasive abilities of human hepatocellular carcinoma (HCC) using an in vitro cell system.</p><p><b>METHODS</b>The highly metastatic human hepatoma cell line MHCC97-H was transiently transfected with the pcDNA3.1/HisC vector expressing the KiSS-1 gene (experimental group) or the vector without the KisS-1 gene (blank control group). Untransfected cells served as the negative control group. Proliferative abilities of the three groups were assessed by flow cytometry and MTT assay. Adhesive abilities were assessed by MTT assays using matrigel and fibronectin. Invasive abilities and cell motility were assessed by chemoinvasion chamber assay using reconstituted matrigel and migration chamber assay using polycarbonate filters, respectively.</p><p><b>RESULTS</b>The experimental group showed significantly lower adhesion capacity to matrigel (0.257+/-0.029) than either the blank control group (0.374+/-0.016; t=-7.90345, P less than 0.01) or the negative control group (0.394+/-0.031; t=-7.22752, P less than 0.01). Similarly, the experimental group showed significantly lower adhesion capacity to fibronectin (0.292+/-0.004) than either the blank control group (0.394+/-0.010; t=-20.93138, P less than 0.01) or the negative control group (0.412+/-0.023; t=-11.31371, P less than 0.01). The experimental group also showed significantly lower numbers of cells with invasive capacity (42.40+/-1.14) than either the blank control group (66+/-1.58; t=-27.0711, P less than 0.01) or the negative control group (67.80 +/- 1.92; t=-25.4, P less than 0.01). Similarly, the experimental group showed significantly lower numbers of cells with chemotactic movement (65.80+/-1.92) than either the blank control group (93.80+/-2.28; t=-30.11750, P less than 0.01) or the negative control group (96.40+/-2.07; t=-24.19142, P less than 0.01). The experimental group showed slightly, but not significantly, lower cell proliferation (0.644+/-0.027) than either the blank control group (0.669+/-0.022; t=-1.60371, P?>?0.05) or the negative control group (0.678+/-0.027; t=-1.97828, P?>?0.05). In addition, there were no obvious differences between the three groups in the amounts of cells arrested in either the G1 phase or the S phase.</p><p><b>CONCLUSION</b>KiSS-1 overexpression suppresses the adhesion, invasion and motility, but not the proliferation, of hepatoma carcinoma cells in vitro. These findings imply that KiSS-1 might represent a promising new candidate for gene therapy against human hepatocellular carcinoma.</p>

Role of mPGES-1 in the occurrence, progression, metastasis and invasion of hepatocellular carcinoma / 中华肝脏病杂志

<p><b>OBJECTIVE</b>To study the expression of mPGES-1 in hepatocellular carcinoma (HCC), observe the effect of MK886 on down-regulation of mPGES-1 gene expression on the biology of human hepatocarcinoma cell line HepG2 and to investigate its significance in the occurrence, progression, metastasis and invasion.</p><p><b>METHODS</b>HCC tissues, para-carcinoma tissues, far-carcinoma tissues and normal liver tissues were collected. The expressions of mPGES-1 were determined by reverse transcription-polymerase chain reaction (RT-PCR) and Western blot. The proliferation, adherence, migration and invasion abilities of HepG2 cells interfered by MK886 were assessed by MTT and transwell technique respectively.</p><p><b>RESULTS</b>The expression of mPGES-1 in HCCs was higher than that in normal liver tissues (P < 0.01), which increased following histological grade. Furthermore, mPGES-1 expression level was higher in the capsule invasion and metastasis tumor than in primary locus. A significant dose-dependent down-regulation of expressions of mPGES-1 gene mRNA and protein were observed in HepG2 cells when MK886 was given for 48 h (F = 140.402, P < 0.01; a'= 0.00714, P < 0.01). Compared with the control group, the growth inhibitory rate of HepG2 cell was observed significantly time and dose-dependent when MK886 was given. The rate of adhesion cells in experimental groups were 85.3% ± 1.3%, 70.5% ± 1.5% and 45.8% ± 2.4%, respectively, less than that in control group 100.0% ± 0 (F = 626.313, P < 0.01). The migration cells was 92.47 ± 1.90, 62.63 ± 1.96 and 37.33 ± 0.83 respectively in the experimental groups after 24 h, lower than that in the control group 128.93 ± 2.60 (F = 1253.805, P < 0.01). The invasion assay revealed that the invading cells were 41.67 ± 1.30, 25.47 ± 1.30 and 13.93 ± 1.66 in the experimental groups, in contrast to 55.67 ± 2.08 in control group after 24 h. The difference between these groups was significant (F = 372.615, P < 0.01). The numbers of adhesion, migration and invasion of HepG2 cells were dose-dependent in MK886 groups.</p><p><b>CONCLUSION</b>Over-expression of mPGES-1 was associated with the tumorigenesis and progression of HCC. The down-regulation of mPGES-1 gene expression might indicated the decrease of the invasion and metastasis of HCC.</p>

Expression of survivin, p27 and PTEN in hepatocellular carcinoma and their clinical significances / 中华肝脏病杂志

<p><b>OBJECTIVE</b>To detect the expression of survivin protein, survivin mRNA, p27 protein, p27 mRNA and PTEN protein in hepatocellular carcinomas (HCC) and their clinical significances.</p><p><b>METHODS</b>Tissue microarrays were constructed. The expression of survivin protein, p27 protein and PTEN protein were evaluated by immunohistochemical methods and in expression of survivin mRNA and p27 mRNA were evaluated by in stiu hybridization respectively in tumor tissues from 141 HCC patients, 128 samples of para-carcinoma liver tissues, 97 liver tissues far from the carcinomas and normal liver tissues from non HCC patients. The relationship of survivin, p27 and PTEN were investigated and a prediction model of HCC was constructed.</p><p><b>RESULTS</b>The expressions of survivin protein (Ridit 95% CI = 0.689+/-0.048, P < 0.01), survivin mRNA (Ridit 95% CI = 0.690+/-0.049, P < 0.01) and p27 protein (Ridit 95% CI = 0.556+/-0.053, P < 0.05) in HCC tissues were significantly increased, while the expression of PTEN protein (Ridit 95% CI = 0.282+/-0.048) in HCC tissues was significantly reduced (P < 0.01).</p><p><b>CONCLUSION</b>Overexpressions of survivin mRNA and p27 protein and reduced expression of PTEN protein might be a valuable marker to predict the presence of HCC.</p>