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1.
AIM: To evaluate the effects of NS-398, a cyclooxygenase-2(COX-2) inhibitor, on the proliferation and apoptosis in HepG2 cells. METHODS: The effects of NS-398 on the proliferation of HepG2 cells was evaluated by MTT. DNA fragmentation gel analysis was used to analyze the apoptotic cells; DNA ploidy and apoptotic cell percentage were examined by flow cytometry. Furthermore, the expression of COX-2 and Bcl-2 mRNA was identified by competitive RT-PCR. RESULTS: NS-398 inhibited cell proliferation and induced apoptosis in HepG2 in a concentration-dependent manner. DNA ploidy analysis showed that S phase cells were significantly decreased with NS-398 concentration increasing. The quiescent G0/G1 phase was accumulated with decreasing of Bcl-2 mRNA. Whereas NS-398 had no effect on the expression of COX-2 mRNA, no correlations were found between COX-2 mRNA and the HepG2 cell proliferation and apoptosis induced by NS-398 (r=0.056 and r=0.119, respectively). CONCLUSION: NS-398 significantly inhibits the proliferation and induces apoptosis in HepG2. Mechanisms may be involved in accumulation of quiescent G0/G1 phase and decrease in Bcl-2 mRNA expression, but independent to COX-2 mRNA expression.  相似文献   

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3.
AIM: To evaluate the growth-inhibitory effects of NS-398, a selective cyclooxygenase-2 inhibitor, in human colon cancer HT-29 cells and its possible mechanisms. METHODS: MTT assay was applied to detect the cell proliferation. Flow cytometry was performed to detect apoptosis rate and cell cycle. RT-PCR was used to detect the expression of bcl-2 mRNA and bax mRNA. Alteration of cytoskeleton component F-actin was observed by confocal laser scanning microscope. RESULTS: NS-398 could inhibit growth of HT-29 cells in dose-and time-dependent manners. Flow cytometry revealed that NS-398 could induce apoptosis and cause G0/G1 arrest of HT-29 cells in a dose-dependent manner. After 72 h incubation with NS-398 at different concentrations, the expression level of bcl-2 mRNA was lowered and the ratio of bcl-2 to bax was decreased in HT-29 cells. F-actin was mainly distributed around nuclei forming annular structure in HT-29 cells. After exposure to NS-398, the annular structure around nuclei disappeared and fluorescence intensity of F-actin decreased obviously. CONCLUSION: NS-398 can inhibit the growth effectively and induce apoptosis in HT-29 cells in vitro, which is associated with the down-regulation of bcl-2 to bax ratio and the disruption of cytoskeleton.  相似文献   

4.
AIM:To investigate the possible role of NS-398, a selective inhibitor of cyclooxygenase-2 enzyme, in radiation-induced apoptosis of human hepatoma cell line HepG2 in vitro. METHODS:Hepatoma cell line HepG2 was treated with various concentrations (25, 50, 100, 200 μmol/L) of NS-398 before MTT assay was used to evaluate the cytotoxicity of NS-398. Transmission electron microscopy (TEM) was used to observe the changes of apoptosis in morphology. FCM was performed to quantify the apoptotic percentage. Real-time PCR was used to detect the expression of bcl-2, bax and caspase-3 mRNA, Western blotting was used to measure the expression of Bcl-2 and bax protein, and colorimetric method was provided to analyze the change of caspase-3 activity. RESULTS:The cytotoxicity of NS-398 increased in time-dependent and dose-dependent manners. NS-398 significantly enhanced radiation-induced apoptosis (P<0.01), increased the expression of bax mRNA, Bax protein, caspase-3 mRNA and enhanced caspase-3 activity, whereas no significant change in Bcl-2 expression was found (P>0.05). CONCLUSION:NS-398 enhances radiation-induced apoptosis in hepatoma cell line HepG2. The mechanism may be associated with the up-regulation of the expression of Bax, caspase-3 and enhancement of the activity of caspase-3, which ultimately induce apoptosis in HepG2.  相似文献   

5.
AIM: To characterize the effect of prostatic epithelial cell paracrine on aromatase expression in prostatic stromal cells.METHODS: Conditioned medium (CM) of prostatic epithelial cell lines (BPH-1, LNCap, DU-145 and PC3) were collected and used to treat prostatic stromal cells. Expression of aromatase was determined by real-time RT-PCR and Western blotting. Expression of cyclooxygenase-2 mRNA in prostatic epithelial cell lines and prostaglandin (PGE2) in CMs were examined by real-time RT-PCR and ELISA, respectively. The CM of BPH-1 cells cultured with NS-398, specific inhibitor of cyclooxygenase-2, were collected, and the effect of NS-398 and PGE2 on aromatase expression was analyzed.RESULTS: CM of human benign prostate hyperplasia epithelial cell line (BPH-1) stimulated expression of aromatase mRNA and protein in stromal cells. But CM of prostate cancer epithelial cell lines (LNCap, DU145, PC3) had no effect on aromatase expression. COX-2 mRNA level in BPH-1 was much higher than that of other cell lines and PGE2 concentration in BPH-1 CM was much higher than that of other CMs. PGE2 concentration of the CM from BPH-1 cultured with NS-398 significantly decreased. CM from BPH-1 cultured with NS-398 failed to stimulate aromatase expression, while PGE2 induced aromatase expression in prostatic stromal cells.CONCLUSION: BPH-1 could induce aromatase expression in prostatic stromal cells through paracrine of PGE2.  相似文献   

6.
AIM: To study the effect and mechanism of yeast cytosine deaminase/ thymidine kinase (yCD/TK) double suicide gene driven by alpha fetoprotein (AFP) promoter on hepatocellular carcinoma (HCC) in vitro and in vivo. METHODS: The expression plasmid with yCD/TK double suicide gene, which was driven by AFP promoter, was constructed. HepG2 (AFP positive) and SMMC7721 (AFP negative) human HCC cell lines were both transfected with the above-mentioned expression plasmid through cationic liposome. The cells were treated with 5-fluorocytosine (5-FC) and/or ganciclovir (GCV) at different concentrations. The cell proliferation and cell cycle phase were evaluated by MTT test and flow cytometry respectively. The effect of double suicide gene on HCC xenografts in nude mice was observed through measuring the tumor size and the number of apoptosis cells. RESULTS: The double suicide gene was expressed selectively on HepG2 cells, rather than on SMMC7721 cells. The 5-FC and/or GCV inhibited effectively the proliferation of HepG2 cells in a dose-dependent manner, but had no influence on SMMC7721 cells. The inhibitory effect on HepG2 cells among different treatments was GCV+5-FC>5-FC>GCV. In vivo, the treatments inhibited markedly the growth of HepG2 cell xenografts in nude mice, transfected with yCD/TK gene. More apoptotic cells were found in HepG2 xenografts after the treatment. However, the growth of SMMC7721 cell xenografts could not be inhibited by this double suicide gene therapy, and few apoptotic cells were found. CONCLUSION: yCD/TK double suicide gene driven by AFP promoter has a significant efficacy in treatment of AFP positive HCC. Cell apoptosis may be an important mechanism of yCD/TK double suicide gene-inhibiting the growth of HCC.  相似文献   

7.
AIM: To study the anti-invasive effect of NS-398 on colon cancer cell line HT-29 in vitro an its regulation by CD44v6 and nm23-H1 genes. METHODS: Flow cytometry was used to detect the expression of COX-2 and CD44v6 in HT-29 cells. MTT was used for cell survival rate tests. The modified Boyden chamber model was used for quantitative invasion assay. RT-PCR was used to detect the expression of nm23-H1 mRNA. RESULTS: Flow cytometry analysis showed that COX-2 was positive in HT-29 cells. NS-398 had significant inhibitory effects on invasion of HT-29 cells, which had no relation with its cytotoxicity. NS-398 down-regulated the expression of CD44v6 and up-regulated the expression of nm23-H1 mRNA. CONCLUSION: NS-398 has an anti-invasive effect on HT-29 cells in vitro. Down-regulation of CD44v6 and up-regulation of nm23-H1 may be its underlying mechanisms.  相似文献   

8.
AIM: To determine the inhibition of VEGF small interfering RNA (siRNA) on expression of VEGF protein and SMMC 7721 cell growth. METHODS: Nine VEGFsiRNA sequences with nineteen nucleotides were designed under the assistance of computer. The inhibitory effect of VEGFsiRNA was analyzed by CCK8. The protein level of VEGF in the media was determined by ELISA. The change of cell cycle was detected by flow cytometry. RESULTS: All the VEGFsiRNA were capable of inhibiting the proliferation of SMMC 7721 cells significantly compared with control and lipofectamine control, while the inhibitory effects of VEGFsiRNA2, VEGFsiRNA4, VEGFsiRNA6, VEGFsiRNA7, VEGFsiRNA8 and VEGFsiRNA9 were better than that of antisense oligodeoxynucleotide. All the VEGFsiRNA reduced the expression of VEGF protein. The effect of VEGFsiRNA7 and VEGFsiRNA2 were the best with the inhibitory rates of 52.65% and 50.43%， respectively. VEGFsiRNAs induced the S arrest in SMMC 7721 cells. The signs of apoptosis in SMMC 7721 cells induced by VEGFsiRNA were not observed. CONCLUSION: VEGFsiRNA sequences were designed and synthesized successfully. VEGFsiRNA effectively inhibited the proliferation of SMMC 7721 cells and reduced the level of VEGF protein.  相似文献   

9.
AIM: To investigate the inhibitory effects of recombinant human Mullerian inhibiting substance on cell proliferation in human ovarian carcinoma cells (OVCAR8 and SKOV3 cell lines). METHODS: The expression of MISIIR protein and the localization of MISIIR protein were analyzed by Western blotting and confocal spectral microscopy, respectively. Cell apoptosis and cell cycle were detected by flow cytometry (FCM). Cell viability was determined via MTT method. Clone formation test was used to detect oncogenicity in vitro.RESULTS: The MISIIR protein expression in OVCAR8 cells but not in SKOV3 cells was observed. MISIIR expression was seen on the OVCAR8 cell surface and in the cytoplasm with both antibodies. After treated with rhMIS for 48 h, the cell viability was significantly decreased in OVCAR8 cells. rhMIS inhibited the oncogenicity of OVCAR8 cells greatly. The cell apoptosis of OVCAR8 cell exposed to 10 mg/L rhMIS was (31.3±2.1)%, and OVCAR8 cells in the G1 phase were increased by (70.4±3.0)%. Compared to SKOV3 cells the differences were significant (P<0.01). CONCLUSION: Recombinant human Mullerian inhibiting substance suppresses the growth of MISIIR-positive ovarian cancer cells by inducing apoptosis and cell cycle arrest. We predict that rhMIS might be a new target to treat human ovarian malignancies.  相似文献   

10.
Abstract: AIM: To investigate the effects of esophageal cancer-related gene 2 (ECRG2) protein combined with cisplatin (DDP) on the proliferation and apoptosis of human esophageal cancer EC9706 cells. METHODS: Methylthiazolyl tetrazolium (MTT) assay was used to examine the effects of single ECRG2 protein and ECRG2 protein combined with DDP on the proliferation of EC9706 cells. Hoechest 33258 staining was applied to analyze the effect of single ECRG2 protein and ECRG2 protein combined with DDP on apoptosis of EC9706 cells. The expression of p53 in EC9706 cells was detected by Western blotting. RESULTS: ECRG2 protein inhibited the proliferation of EC9706 cells. ECRG2 protein combined with DDP enhanced the inhibitory effect time- and dose-dependently in a certain range of concentrations. The number of apoptotic cells after treated with ECRG2 protein combined with DDP for 24 h was larger than those treated with single ECRG2 protein. The proliferation-inhibitory and qpoptosis-inducing expression of p53 was up-regulated in ECRG2 protein and DDP combination group compared with single ECRG2 protein group. CONCLUSION: DDP enhances the proliferation-inhibitory and apoptosis-inducing effects of ECRG2 protein on EC9706 cells. The apoptosis-inducing mechanism may be related to the up-regulation of p53 expression.  相似文献   

11.
AIM: To clarify the effects of specific and non-specific cyclooxygenase-2 (COX-2) inhibitors on gastric epithelial cell proliferating and gastric healing following acid-induced damage. METHODS: Male Sprague-Dawley rats were given 1 mL of 0.6 mol/L hydrochloric acid (HCl) into the stomach. Ten minutes after the administration of the acid, the animals were given NS-398 (COX-2 inhibitor) or indomethacin. Levels of COX-1 and COX-2 in the gastric mucosa before and after HCl-administration were analyzed using western blotting and immunohistochemical staining. Proliferating cell nuclear antigen (PCNA) was detected using immunohistochemistry for epithelial cell proliferation. Gastric lesion index (LI) was assessed using planimetry. RESULTS: Expression of COX-2 was enhanced mainly in surface epithelial cells and neck cells following HCl-administration. At 24 h following acid administration, PCNA labeling index (PCNA-LI) was (22.72±4.33) % and (21.98±5.18) % in the groups treated with 40 mg/kg of NS-398 and indomethacin respectively, which was significantly lower than that in the control group [ (34.46±3.61) %, P< 0.05 ]; LI was (1.28±0.58) % and (1.16±0.56) % in the groups treated with 4 mg/kg and 40 mg/kg of NS-398, respectively, which was significantly higher than that in the control group [ (0.58±0.24) %, P< 0.05 ]. CONCLUSIONS: The present study demonstrated that cyclooxygenase-2 inhibitors delayed gastric mucosal healing by suppressing expansion of the mucosal proliferative zone. These results provide evidence that cyclooxygenase-2 plays an important role in gastric mucosal regeneration.  相似文献   

12.
AIM: To investigate the change of chemosensitivity of esophageal carcinoma cells before and after induction by radiation,and to detect the excision repair cross complementation group 1 (ERCC1) gene before and after induction,and further to analyze the relationship between ERCC1 expression and chemosensitivity.METHODS: The esophageal carcinoma cell EC9706 was radiated repeatedly by a long-term,intermittent ［60Co］-γ radiation to induce the radioresistance esophageal carcinoma cell EC9706-R.The IC50 and resistant index (RI) of EC9706 and EC9706-R were detected by MTT assay.The expression of ERCC1 was examined by immunocytochemistry and RT-PCR.RESULTS: The IC50 of EC9706 and EC9706-R cells to cisplatin were (1.480±0.012) mg/L and (1.836±0.008) mg/L,respectively (P<0.05),and the RI was 1.240±0.015.The tinctorial scores of ERCC1 protein in EC9706 and EC9706-R were 2.838±0.055 and 2.898±0.039 (P>0.05),and the relatively quantities (IDV) of ERCC1 mRNA in EC9706 and EC9706-R cells were 1.168±0.068 and 1.143±0.089 (P>0.05).SP and RT-PCR did not display visible difference in protein level and mRNA level.CONCLUSION: The chemosensitivity of EC9706-R cells to cisplatin is decreased compared with EC9706 cells,but ERCC1 expression does not change with the radioresistance and chemoresistance.  相似文献   

13.
AIM: To investigate the effect of microRNA-24-3p (miR-24-3p) on the viability and apoptosis of esophageal cancer cells. METHODS: The expression of miR-24-3p and KLF6 mRNA in the esophageal cancer cells TE11, Eca109 and EC9706 were detected by RT-qPCR. The protein expression of KLF6 was determined by Western blot. EC9706 cells were transfected with anti-miR-24-3p and KLF6 siRNA. The cell viability was measured by MTT assay, the apoptotic rate was analyzed by flow cytometry, and the proliferation, apoptosis and IL-6/STAT3 signaling pathways related proteins were determined by Western blot. The level of IL-6 was measured by ELISA. The dual luciferase reporter gene assay was used to verify the relationship between miR-24-3p and KLF6. RESULTS: The levels of miR-24-3p were up-regulated in the esophageal cancer cells TE11, Eca109 and EC9706 (P < 0.05), and the expression of KLF6 at mRNA and protein levels was down-regulated (P < 0.05). Knock-down of miR-24-3p expression inhibited the cell viability, induced apoptosis, and inhibited the protein levels of CDK4, cyclin D1, CDC25A, p-STAT3, Bcl-2 and IL-6, and promoted the protein expression of caspase-3 and Bax in EC9706 cells. CONCLUSION: miR-24-3p targets KLF6 gene to affect the viability and apoptosis of esophageal cancer cells by regulating IL-6/STAT3 signaling pathway.  相似文献   

14.
AIM: To investigate the effects of silencing of cyclooxygenase-2 (COX-2) gene expression by siRNA on the proliferation, apoptosis, cell cycle and tumorigenicity of human pancreatic cancer Capan-2 cells.METHODS: The gene transfection was performed using Lipofectamine 2000 (Lipo). The proliferation, apoptosis and cell cycle of Capan-2 cells were tested by the methods of cell counting, microscopy and FCM. The mRNA expression of COX-2 was determined by RT-PCR and real-time PCR. The protein level of COX-2 was detected by Western blotting. The tumorigenicity of Capan-2 cells transfected with siRNA-COX-2 was determined using the model of nude mice. RESULTS: Transfection efficiency of 96.47% was obtained under the conditions that the transfection volume was 2 mL, concentration of Lipo was 5 μL and that of siRNA-COX-2 was 50 nmol/L. The best sequence of siRNA-COX-2 for silencing of COX-2 gene expression was siRNA006 with the silencing rate of up to 73% 24 h after tansfection. siRNA-COX-2 slowed down the growth of Capan-2 cells 48 h after transfection (P<0.05). At time points of 48 h and 72 h after transfection, the protein expression of COX-2 was down-regulated to 67% and 61% of the normal level, the proliferation inhibition rate was 35.48% and 56.32%, and the apoptotic rate was 2.03% and 3.27%, respectively. At time points of 24 h, 48 h and 72 h after transfection, the proportion of the cells in G0/G1 phrase was 58.03%, 63.31% and 65.66%, and that of the cells in S phase was 30.27%, 24.87% and 22.2%, respectively. The mean volume and weight of tumor tissues were remarkably decreased due to the transplantation of Capan-2 cells transfected with siRNA-COX-2.CONCLUSION: siRNA-COX-2 effectively silences the expression of COX-2 gene, inhibits the growth and decreases the tumorigenicity of Capan-2 cells.  相似文献   

15.
AIM: To investigate the expression of immunoglobulin G (IgG) in bladder transitional carcinoma cells (BTCC) and the effect of the antibody against human IgG on tumor cell apoptosis.METHODS: The expression of IgG of BTCC was detected by immunohistochemistry, Western blotting, enzyme linked immunosorbent assay (ELISA) and flow cytometry (FCM). The expression of IgG mRNA was tested by hybridization in situ method and RT-PCR in vitro. Antiproliferation effects of the antibody of antihuman IgG on T24 and BIU-87 cell lines were measured by MTT assay. Cell apoptosis was assessed by FCM.RESULTS: The expression of IgG was 91.1％ (51/56) in clinical cases, and 45.4％ (5/11) in normal controls. Immunohistochemistry and Western blotting showed that the IgG was significantly expressed in T24 and BIU-87. FCM indicated the IgG was mainly expressed in cytoplasma. No IgG was detected by ELISA in supernatant of cell culture medium. RT-PCR and hybridization in situ demonstrated IgG mRNA was significantly expressed in two cell lines. Under the treatment of 25 mg/L of goat nonspecific IgG and the antibody of antihuman IgG, the inhibition ratio of cell growth in T24 and BIU-87 were (4.73±3.73)% vs (24.98±3.81)% and (5.36±1.53)% vs (22.70±3.72)%, respectively (P<0.05). The percentages of apoptotic cells in T24 and BIU-87 were 2.3% vs 20.7% and 1.3% vs 15.3%, respectively.CONCLUSION: IgG is significantly expressed in bladder transitional carcinoma cell. The antibody of antihuman IgG inhibits cancer cell growth and induces tumor cell apoptosis.  相似文献   

16.
AIM: To explore the effect of N-cadherin knock-down on the biological behavior of EC9706 cells in vivo.METHODS: The control vector pEGFP-MSCVneo and recombinant retroviral vector pMSCVneo/N-cadherin plasmids were transfected into esophageal squamous cell carcinoma(ESCC) cell line EC9706 according to the manufacturer's instructions. Stable EC9706 cell clones were selected using selection medium containing G418. Untreated EC9706 cells, control vector-transfected EC9706 cells and N-cadherin RNAi-transfected EC9706 cells were inoculated subcutaneously into the right flank of BALB/c mice (5 for each group), respectively. When tumors became palpable, the diameters of the tumors were measured with a caliper each week after subcutaneous implantation, and the volume (mm3) and weight (g) of the tumors were also calculated. Immunohistochemistry and Western blotting were employed to examine the expression levels of E-cadherin, N-cadherin and MMP-9 in the tumor tissues. The cell apoptosis was analyzed by TUNEL method.RESULTS: Compared with untreated group and control vector group, there was an obvious decrease in the volumes and weights of the tumors in N-cadherin RNAi group (P<0.05). No difference of E-cadherin expression in the 3 groups was observed. However, the expression of N-cadherin and MMP-9 in N-cadherin RNAi group was apparently reduced, and the positive number of cell apoptosis was obviously increased in N-cadherin RNAi group (106.81±6.47) as compared with that in untreated group (51.55±4.68) and control vector group (54.17±5.26). CONCLUSION: N-cadherin knock-down inhibits the tumor formation of EC9706 cells in nude mice by decreasing MMP-9 expression, resulting in less degradation of ECM and less aggression of the cancer cells. N-cadherin is an important factor in the progression and metastasis of ESCC,and may serve as a potential molecular target for biotherapy of ESCC.  相似文献   

17.
AIM: To investigate the effect of human chorionic gonadotropin(hCG) on cyclooxygenase-2(COX-2) expression in endometrial carcinoma so as to study the function of ectopic hCG.METHODS: The ectopic β-hCG in JEC endometrial carcinoma cell lines was quantified by radioimmunoassay. By MTT assay, the effect of hCG on the cell viability of JEC cell lines and the inhibition of selective COX-2 inhibitor NS398 on JEC cell lines were examined. The effect of hCG on COX-2 expression was detected by Western blotting. RESULTS: The ectopic β-hCG release from cultured JEC cell lines were observed. HCG promoted the cell viability, upregulated the expression of COX-2 protein and increased the inhibition of selective COX-2 inhibitor NS398 in JEC cell lines. CONCLUSION: The ectopic hCG in JEC endometrial carcinoma cell lines increases cell proliferation, which may be mediated by upregulating the expression of COX-2 protein.  相似文献   

18.
AIM: To investigate the effect on growth and activity of telomerase in esophageal carcinoma cells by inhibiting ubiquitin-proteasome pathway(UPP). METHODS: The esophageal carcinoma cell strain Eca9706 was treated with MG-132 to inhibit its UPP specially. The effect of growth suppression on cells was evaluated with MTT assay, morphologic changes of cells were observed under microscope, cell cycle and apoptosis were detected by flow cytometry (FCM). DNA fragment analysis was used to confirm the presence of apoptosis. The activity of telomerase was detected. RESULTS: MG-132 had obvious inhibitory effect on the growth of Eca9706 cells in a dose and time-dependent manner. Obvious pathologic change of cells were observed under microscope, cells became round, small and exfoliating. The FCM analysis showed that the ratio of esophageal carcinoma cells of G1 phase increased and a obviously apoptotic sub-G1 peak was found. Agarose electrophoresis showed marked ladder. The activity of telomerase was obviously inhibited. CONCLUSIONS: MG-132 significantly inhibits the growth and the activity of telomerase of Eca 9706 cells. These findings indicate that inhibiting UPP is a new strategy for the treatment of esophageal carcinoma.  相似文献   

19.
AIM: To evaluate the role of natural killer(NK) cells against a variety of human hepatocellular carcinoma (HCC) cell lines in vitro and in vivo, and to investigate the expression of MHC class I chain-related protein (MIC protein) in these HCC cell lines. METHODS: Peripheral blood mononuclear cells (PBMC) were isolated from 50 mL peripheral blood donored by a healthy volunteer and cultured in the NK cell kit followed by amplification and cytokine activation. The release of lactate dehydrogenase (LDH) was detected by lysis experiment. Animal experiments were performed following vaccination with HCC cell lines (BEL7402, HepG2 and SMMC7721) in BALB/c-nu/nu mice. The diameters of the tumors were measured and the growth curves of difference cell lines were delineated. Three weeks later, these mice were sacrificed and the weight of the transplanted tumors was also detected. Furthermore, the expression of MIC protein was determined. RESULTS: The obvious differences of lysis effects of NK cells on different cell lines were observed, in which the lysis effect of NK cells on K562 cells was the strongest, the effect on BEL7402 cells was in the middle and the effect on SMMC7721 cells was the weakest. In animal experiments, NK cells also showed obvious and different restraining effects on a variety of HCC cell line-transplanted tumors in nude mice. The tumor inhibitory rates of NK cells were 43.5% in BEL-7402 cell-transplanted tumor, 40.7% in HepG2 cell-transplanted tumor and 36.0% in SMMC-7721 cell-transplanted tumor. The protein expression of MIC was 48.7%, 32.8% and 0.9% in the 3 cell lines,respectively. CONCLUSION: The lysis effects of NK cells on a variety of human HCC cell lines are different. The expression of MIC in the tumor cells may play distinct role in evaluating these differences.  相似文献   

20.
AIM: To study the expression and characterization of intracellular macrophage colony-stimulating factor (M-CSF) in human hepatoma cell line, SMMC 7721 cell, and to explore the mechanism by which M-CSF regulates the proliferation of human hepatoma cells. METHODS: The immunohistochemical staining, flow cytometry, antisense technique and Western blotting were used to study the effects and mechanisms of intracellular M-CSF on the proliferation of human hepatoma cells. RESULTS: SMMC 7721 cells highly expressed M-CSF and its receptor. The localization of positive reactions was mainly in cytoplasma and nucleus in SMMC 7721 cells. In cytoplasma and nucleus, one isoforms of M-CSF was found with the molecular weight (MW) of 20 kD, while one type of M-CSFR was discovered with MW of 120 kD. Immunoprecipitation assay showed that these ligands existed in binding with its receptor. Monoclonal antibody (McAb) against M-CSF and antisense oligodeoxynucleotides (ASODN) blocking M-CSF expression inhibited the proliferation of SMMC 7721 cells. McAb and ASODN regulated the expression of cyclin D1/E and p16. Simultaneous administration of both McAb and ASODN inhibited the proliferation of SMMC 7721 cells and modulated the expression of cyclins at greater degrees. CONCLUSION: Our results suggest that an autocrine and an intracrine loop of M-CSF/M-CSFR are present in SMMC 7721 cells.  相似文献   

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