Effects of NS-398 on the proliferation and apoptosis of HepG2 cells

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.     

Effects of shRNA targeting SIAH2 gene on proliferation and apoptosis of human hepatoma cell line HepG2

AIM：To investigate the effects of shRNA-mediated seven in absentia homolog 2 (SIAH2; one of ubiquitin ligases) gene silencing on cell cycle and apoptosis of human hepatoma cell line HepG2. METHODS：The specific recombinant vector pGenesil-SIAH2 was transiently transfected into HepG2 cells with Lipofectamine 2000. RT-PCR and Western blotting were performed to detect the mRNA and protein expression levels of SIAH2. MTS assay was employed to evaluate the cell proliferation. Flow cytometry was used to determine the cell cycle and apoptosis of the transfected cells. RESULTS：Compared with control groups, the mRNA and protein levels of SIAH2 were reduced by pGenesil-SIAH2 transfection in HepG2-SIAH2 group. The proliferation of HepG2-SIAH2 cells was significantly inhibited. The percentage of G1-phase cells and the early apoptotic rate were significantly higher in HepG2-SIAH2 cells. CONCLUSION: Tansfection of pGenesil-SIAH2 effectively inhibits the proliferation of HepG2 cells, arrests the cells in G1 phase and induces apoptosis, indicating an experimental basis of SIAH2-targeting gene therapy for hepatocellular carcinoma.     

Over-expression of GSTP1 increases oxaliplatin-induced apoptosis in human hepatoma HepG2 cells

AIM: To investigate the effect of GSTP1 over-expression on the sensitivity of human hepatoma HepG2 cells to oxaliplatin (OXA). METHODS: Adenovirus carrying GSTP1 (Ad-GSTP1) was used to infect HepG2 cells for establishing the cell line over-expressing GSTP1. The cells were randomly divided into 6 groups:control, vehicle, Ad-GSTP1, OXA, OXA+vehicle and OXA+Ad-GSTP1. The cell survival rates were examined by CCK-8 assay, and the apoptotic rates were analyzed by flow cytometry. The protein levels of GSTP1, Akt, mTOR, p-Akt and p-mTOR were determined by Western blot. RESULTS: OXA decreased the cell survival rate in a dose-dependent manner (P<0.05). The protein expression of GSTP1 increased after transfection with adenovirus. At basal level, up-regulation of GSTP1 significantly decreased the cell survival rate, increased the cell apoptosis, and inhibited the phosphorylation levels of Akt and mTOR (P<0.05). Moreover, GSTP1 over-expression enhanced the effect of OXA on the cell viability, cell apoptosis, and further inhibited the phosphorylation levels of Akt and mTOR (P<0.05).CONCLUSION: Over-expression of GSTP1 augments the enhanced effect of OXA on HepG2 cell apoptosis, which may be related to the inactivation of Akt/mTOR signaling pathway.     

In vitro killing effect of adenovirus-mediated herpes simplex virus thymidine kinase gene under regulation of hypoxic response element on hepatoma cell line HepG2

AIM: To investigate the in vitro killing effect of adenovirus-mediated herpes simplex virus thymidine kinase gene (HSV-TK) driven by hypoxic response element (HRE) on hepatoma cell line HepG2. METHODS: Recombinant adenoviral vector Ad-HRE-TK was constructed with HSV-TK under the control of HRE using AdEasy system. Then Ad-HRE-TK was transfected into hepatoma cell line HepG2 and the cells were cultured under normoxic or hypoxic conditions. After treated with GCV for 3 d, the sensitivity to GCV of HepG2 was measured by MTT method. RESULTS: Over 95% HepG2 cells infected with Ad-HRE-TK cultured under hypoxic condition were killed when the MOI was 100 and the concentration of GCV was 50 mg/L. On the contrary, no killing effect of GCV was observed in cells cultured under normoxic condition. CONCLUSION: HRE promotes the expression of HSV-TK specifically under hypoxic condition and induces the specific killing effect of GCV.     

Inhibitory effects of a cyclooxygenase-2 inhibitor,NS398,on cancer cells

AIM:To study the mechanism of growth inhibitory effect of a selective cyclooxygenase-2 (COX-2) inhibitor,NS-398,on cancer cells.METHODS:The esophageal cancer cell line (EC9706),which expresses COX-2 constitutively,and hepatocellular carcinoma cell line (SMMC7721),which expresses no COX-2,were studied.The cell lines were incubated with NS-398 at doses of 10,20,50,100 μmol/L for 24 h,48 h and 72 h.Antiproliferation effect was measured by ［3H］-TdR incorporation.The cell apoptosis were determined by flow cytometry (FCM) and DNA fragmentation analysis.Survivin was detected by immunocytochemical technique.RESULTS:The growth inhibition was induced by NS398 in a dose- and time-dependent manners in both cell lines.FCM analysis revealed a high sub-G1 cell peak in EC9706 group and agarose electrophoresis showed marked apoptosis ladder pattern.However,no apoptosis was observed in SMMC7721 cells treated with NS-398.The difference of apoptosis percentage in EC9706 and SMMC7721 was (45.23±1.08)% and (3.05±0.15)% (P<0.01).After 24 h incubation with NS-398 at concentration of 100 μmol/L,the expression of survivin was markedly reduced in EC9706,no change was observed in SMMC7721.CONCLUSION:NS-398 suppresses cell growth in cancer cell lines by different mechanism.NS-398 suppresses cell growth and increases apoptosis in the cancer cells that expresses COX-2.     

Effect of Aurora protein kinase inhibitor VX-680 on homogeneity adhesion and migration in human hepatoma HepG2 cell

AIM:To study the effect of Aurora protein kinase inhibitor VX-680 on homogeneous adhesion and migration ability in human hepatocellular carcinoma cell line HepG2. METHODS:The HepG2 cell were divided into experimental group and control group, respectively. VX-680 was used in experimental groups at 3 concentrations (3.125 μmol/L group, 6.25 μmol/L group and 12.5 μmol/L group). DMSO was used in the control group. The effects of VX-680 at different concentrations on the adhesion ability of human hepatocellular carcinoma HepG2 cells were observed by cell slow aggregation test and separation experiment. The effects of VX-680 at different concentrations on the migration ability of HepG2 cells was detected by wound healing assay. The expression of E-cadherin in HepG2 cells was detected by Western blot. RESULTS:The results of the slow aggregation test showed that compared with the control group, the number of cell clumps formed in experimental groups was significantly decreased (P<0.01). The results of separation experiment showed that the ratio of N_TC/N_TE gradually decreased with the increased concentration of VX-680. The results of wound healing assay showed that as the concentration of VX-680 increased, the cell scratch healing ability gradually weakened compared with control group. The results of Western blot showed that the protein expression of E-cadherin in the HepG2 cells increased with the increased concentration of VX-680 (P<0.05). CONCLUSION:VX-680 increases the homogeneous adhesion and inhibits the migration of HepG2 cells.     

Effects of 2-deoxy-D-glucose and oxaliplatin on proliferation and apoptosis of human hepatoma cell line SMMC-7721

AIM: To investigate the effects of 2-deoxy-D-glucose (2-DG) or oxaliplatin (L-OHP) alone and the combination of both on the proliferation and apoptosis of hepatoma cell line SMMC-7721 in vitro. METHODS: Human hepatoma cell line SMMC-7721 was treated with 2-DG or L-OHP alone, or both. The inhibitory effect on the proliferation of SMMC-7721 cells was estimated by MTT method. The q value, which represents synergistic effect, was determined. Apoptotic rate and cell cycle were assayed by flow cytometry. The activity of caspase-3 was detected by a caspase-3 activity assay kit. RESULTS: 2-DG or L-OHP at different concentrations inhibited the growth of SMMC-7721 cells obviously and the inhibitory effect on SMMC-7721 cell growth strongly depended on the exposure time and dose. When the 2 drugs worked together, the inhibitory effect was improved (P<0.05). 2-DG induced cell apoptosis and arrested the cells at G₂/M phase. When combined with L-OHP,the 2 drugs induced more severe apoptosis and arrested the cells at S and G₂/M phase. Meanwhile, the activity of caspase-3 increased when the 2 drugs used together. CONCLUSION: 2-DG inhibits the growth of hepatoma cell line SMMC-7721. The combination of 2-DG and L-OHP improves the ability of L-OHP to attack the tumor cells. The mechanism might be related to increasing the activity of caspase-3.     

Effects of sulphated heparin on proliferation and apoptosis of human hepatocellular carcinoma cell line (HepG2)

AIM:To explore the effect and the mechanism of sulphated heparin on the proliferation and the apoptosis of human hepatocellular carcinoma cells.METHODS:The human hepatocellular carcinoma cell line (HepG-2) was used to identify the expression ofrasgene protein and to study the effect of sulphated heparin on proliferation and the apoptosisin vitro.RESULTS:The sulphated heparin downregulated the ras protein expression and inhibited the cell growth in HepG2 cells. In the presence of sulphated heparin, the apoptosis rate of HepG2 increased.CONCLUSION:The data suggest that the effects of sulphated heparin on the proliferation and the apoptosis of the human hepatocellular carcinoma cell are correlated with the signaling transduction mediated byrasgene protein.     

Effects of XPD on expression of Rb and MAD2 in human hepatoma HepG2 cells

AIM：To investigate the effects of xeroderma pigmentosum group D (XPD) protein on the growth of human hepatoma HepG2 cells and the expression of retinoblastoma (Rb) and mitotic arrest deficient 2 (MAD2) proteins. METHODS：The recombinant plasmid pEGFP-N2-XPD and empty plasmid pEGFP-N2 were transfected into HepG2 cells by LipofectamineTM 2000. The cells were divided into 4 groups including blank control group, liposome group, pEGFP-N2 group (N2 group) and pEGFP-N2-XPD group (XPD group). The expression of XPD, Rb and MAD2 at mRNA and protein levels was detected by RT-PCR and Western blotting. The cell growth was measured by MTT assay. The cell apoptosis and cell cycle were analyzed by flow cytometry. RESULTS：Overexpression of XPD up-regulated the expression of Rb, and down-regulated the expression of MAD2 at mRNA and protein levels. XPD inhibited the proliferation of HepG2 cells and exacerbated the apoptosis. XPD prevented the hepatoma cells from G1 stage to S stage. CONCLUSION：XPD suppresses the growth of hepatoma cells, up-regulates the expression of Rb, and down-regulates the expression of MAD2.     

Thapsigargin inhibits growth and induces apoptosis in human len epithelial cell line HLE-B3 in vitro

AIM: To study the effect of growth inhibition and its mechanism of thapsigargin (TG) on HLE-B3 cell line in vitro. METHODS: MTT assay was performed to detect the growth inhibition effect of TG on HLE-B3 cell line. Flow cytometry and DNA fragmentation were used to examine cell apoptosis. Western blotting analysis was used to determine the relative protein expression. Furthermore, the concentration of cytoplasm Ca2+ was assessed by fluorescence colorimetric assay. RESULTS: Different concentrations of TG significantly inhibited growth of HLE-B3 cells, and inhibitory concentrations of 50 percent at 12 h, 24 h and 48 h were (2.27±0.61) μmol/L, (0.77±0.12) μmol/L and (0.15±0.04) μmol/L, respectively. Moreover, TG induced cell apoptosis, decreased SERCA2 protein expression, and increased greatly the concentration of cytoplasm Ca2+, Bax and caspase 3 protein levels.CONCLUSION: TG inhibits growth and induces apoptosis in HLE-B3 cells in vitro. The mechanism may be through endoplasmic reticulum pathway. These observations may provide a novel strategy for the treatment of posterior capsular opacification.     

Effect of KLF6 gene on nucleotide excision repair capacity in human hepatocellular carcinoma cell line HepG2

AIM: To investigate the roles of KLF6 gene on nucleotide excision repair capacity of human hepatocellular carcinoma cell line HepG2. METHODS: Expression of KLF6 was detected by RT-PCR and Western blotting, followed by HepG2 cells treated with cisplatin (5 mg/L). Host cell reactivation assay was used to assess nucleotide excision capacity of cisplatin-damaged HepG2 cells.RESULTS: Upregulation of KLF6 mRNA or protein in HepG2 cells treated with 5 mg/L concentration of cisplatin was in a time-dependent manner, but KLF6 protein was degraded when exposed to cisplatin at same dose (5 mg/L) for 36 h. HCR assay showed that NER capacity of KLF6 overexpressing HepG2 cells was significantly enhanced, compared to that in control cells. CONCLUSION: DNA damage induced by cisplatin induces the expression of KLF6 gene. KLF6 gene may play an important role in mechanism of nucleotide excision repair in HepG2 cells.     

Effect of Rip2 overexpression on apoptosis in human pancreatic cancer cell line Panc-1

AIM: To observe the effect of receptor-interacting protein 2 (Rip2) overexpression on human pancreatic cancer cell line Panc-1. METHODS: pEGFP-C2 and pEGFP-Rip2 plasmids were respectively transfected into the Panc-1 cells using JetPRIME reagent. The cells were divided into control group, pEGFP-C2 group and pEGFP-Rip2 group. The apoptosis in the cells was detected 48 h after transfection by flow cytometry. Rip2 level and the expression of apoptosis-related proteins, Bax, cytoplasmic cytochrome c (Cyt-c) and Bcl-2, were analyzed by Western blot. The activity of caspase-3 was measured by colorimetric method. RESULTS: Rip2 protein expression significantly increased in the cells transfected with control and pEGFP-C2 plasmids. The apoptotic rate in pEGFP-Rip2 group was higher than that in control group and pEGFP-C2 group, whereas no significant difference of apoptotic rate was observed between control group and pEGFP-C2 group. The protein expression of Bax and cytoplasmic Cyt-c was remarkably increased and the protein expression of Bcl-2 was obviously decreased in pEGFP-Rip2 group as compared with control group and pEGFP-C2 group. The activity of caspase-3 in pEGFP-Rip2 group was obviously increased as compared with control group and pEGFP-C2 group. CONCLUSION: Overexpression of Rip2 is able to induce apoptosis in the Panc-1 cells, and the mechanism may be related to the up-regulation of Bax and cytoplasmic Cyt-c protein expression, down-regulation of Bcl-2 protein expression and enhancement of caspase-3 activity, thus activating intrinsic apoptotic pathway.     

Effect of Ginsenoside Rh2 on apoptosis of human osteosarcoma cell line MG-63

AIM: To investigate the effect of Ginsenoside Rh2(Rh2) on the apoptosis of human osteosarcoma cell line MG-63.METHODS: The cell viability was determined by MTT assay. MG-63 cell apoptotic rate was examined by flow cytometry with Annexin V-PI double staining. The expression of Bcl-2, Bax, cytochrome C(Cyt C) and cleaved caspase-3 were measured by Western blot.RESULTS: Rh2 enhanced the apoptosis of MG-63 cells in a dose-dependent manner. Furthermore, after treatment with Rh2, the release of mitochondrial Cyt C and Bax expression were increased, while Bcl-2 and the ratio of Bcl-2/Bax were decreased as compared with control group(P<0.05). The protein level of cleaved caspase-3 was also increased(P<0.05).CONCLUSION: Ginsenoside Rh2 accelerates the apoptosis of MG-63 cells through mitochondria-dependent pathway, suggesting that Rh2 is a novel approach for the treatment of osteosarcoma.     

In vitro growth inhibition effects of rhHGF/cHGF on SMMC-7721 human HCC cell line

AIM:To examine the effects of recombinant human hepatocyte growth factor(rhHGF) and native calf HGF(cHGF) on SMMC-7721 human hepatocellular carcinoma(HCC) cell line. METHODS:Human HCC cell line culture, photometric assay, and flow cytometric assay were used in this study .RESULTS:A similar type of dose-dependent cell growth inhibition effect on SMMC-7721 human HCC cells by rhHGF(5-20 μg/L) as well as by cHGF(25-100 mg/L) had been found, with the maximal effect at the highest concentration used. Approximately over 50% of the cells treated with rhHGF(5 μg/L, 10 μg/L, 20 μg/L) accumulated in the quiescent G₀/G₁ phase of the cell cycle over incubation periods for 3 d. CONCLUSION:The growth of SMMC-7721 human HCC cells was strongly inhibited by both rhHGF and cHGF. This might be because the cells exposed to HGF became arrested in the G₀/G₁ phase.     

Effect of TNF-related apoptosis-inducing ligand on virus-induced apoptosis in a human islet β cell line

AIM: To study role of TNF-related apoptosis-inducing ligand (TRAIL) in virus-induced apoptosis in a human islet β cell line, CM cell line. METHODS: Using annexin-V assay to compare Coxsackie virus B (CVB)-induced apoptosis with Rubella virus (RV)-induced apoptosis in a CM cell line; using four kinds of soluble receptors of TRAIL and anti-TRAIL McAb to block the virus-induced apoptosis. RESULTS: 5PFU of CVB3 and CVB4 contacted with CM cells for 5 hours , there were more than 30% apoptotic CM cells; 0.01PFU of CVB3 and CVB4 contacted with CM cells for 24 hours, there were more than 80% apoptotic CM cells; 10PFU of CVB3 and CVB4 contacted with CM cells for 24 hours, there were only less than 25% apoptotic CM cells; soluble receptors of TRAIL and anti-TRAIL McAb could block CVB-induced apoptosis. CONCLUSION: CM cell line is more sensitive to CVB and TRAIL plays a role in CVB-induced apoptosis.     

Effect of NANOG silencing on cyclin D1 expression and proliferation in human hepatoma HepG2 cells

AIM:To investigate the effect of NANOG silencing on cyclin D1 expression and proliferation in human hepatoma HepG2 cells. METHODS:Transient transfection of NANOG targeting siRNA into HepG2 cells was performed. The expression of NANOG and cyclin D1 at mRNA and protein levels was detected by real-time PCR and Western blotting. Cell proliferation was examined by CCK-8 assay and colony formation assay, and cell cycle was tested by flow cytometry. RESULTS:After transfection with NANOG-targeting siRNA, the inhibition of NANOG expression was observed. Compared with mock group, the mRNA and protein expression levels of NANOG and cyclin D1 were decreased (P<005). In addition, knockdown of NANOG expression inhibited the cell proliferation and increased the proportion of G 0/G 1-phase cells (P<0.05). CONCLUSION:Silencing of NANOG expression in HepG2 cells causes down-regulation of cyclin D1 expression and decreases the cell proliferation ability.     

Artesunate induces apoptosis of human hepatocellular carcinoma HepG2 cells by increasing generation of reactive oxygen species

AIM: To investigate the effect of reactive oxygen species (ROS) on the apoptosis of HepG2 cells induced by artesunate. METHODS: The effect of artesunate on the viability of HepG2 cells was measured by MTT assay. The morphological changes of the apoptotic cells were observed by the method of Hoechst 33258 fluorescence staining.The apoptosis of HepG2 cells was analyzed by flow cytometry. DCFH-DA was used to detect the changes of ROS generation during the process of apoptosis. The protein levels of Bax, Bcl-2, cleaved caspase-3 and cytochrome C (Cyt C) were determined by Western blot. HepG2 cells were pretreated with apocynin and then Western blot was used to detect the expression of p47^phox and p22^phox, and ROS changes were analyzed by flow cytometry. RESULTS: Compare with control group, the cell viability was obviously inhibited after treatment with artesunate for 24 h (P<0.05). The nuclei were densely stained, and the proportion of apoptotic cells was increased (P<0.05). ROS was increased significantly (P<0.05). The results of Western blot demonstrated that the expression level of Bax was increased, Bcl-2 was decreased, the ratio of Bax/Bcl-2 was increased, and the protein levels of cleaved caspase-3 and Cyt C were increased. Pretreatment with apocynin reduced the expression of p47^phox and p22^phox and the generation of ROS in the artesunate treatment group. CONCLUSION: Artesunate induces the apoptosis of HepG2 cells. The possible mechanism may be related to the increase in the generation of ROS.     

Knockdown of astrocyte elevated gene-1 by siRNA inhibits cell proliferation and induces apoptosis in human neuroblastoma cell line

AIM: To investigate the effect of siRNA-induced astrocyte elevated gene-1 ( AEG-1 ) down-regulation on the proliferation, apoptosis and cell cycle of neuroblastoma cells. METHODS: An siRNA targeting to AEG-1 mRNA (AEG-1 siRNA) was constructed and transfected into neuroblastoma cells with Lipofectamine 2000. A non-specific siRNA (control siRNA) and non-treatment were used as negative control and blank control,respectively . The cell proliferation was detected by MTT method and colony formation assay. The apoptosis and cell cycle were analyzed by flow cytometry. RESULTS: Compared with control groups, the expression of AEG-1 mRNA was evidently declined in the cells transfected with AEG-1 siRNAs (P<0.05). AEG-1 siRNA significantly decreased the cell proliferation. After treated with AEG-1 siRNA for 48 h, the percentage of apoptotic cells was significant increased and the cell cycle was arrested in G₀/G₁ phase compared with the control cells (P<0.05). CONCLUSION: The mRNA expression of AEG-1 is down-regulated by AEG-1 siRNA in neuroblastoma cells. Knockdown of AEG-1 expression in human neuroblastoma cells significantly inhibits cell proliferation and apoptosis, and induces cell arrest in G₀/G₁ phase of the cell cycle.     

Analysis of expressive proteome in human hepatocarcinoma cell HepG2 transfected with miR-26a mimics

AIM: To determine whether microRNA-26a(miR-26a) is involved in development of liver cancer by analysis of proteomic expression profile of human hepatocarcinoma cell HepG2 transfected with miR-26a mimics.METHODS: HepG2 cells were cultured by a routine method and transfected with miR-26a mimics for 48 h for cell cycle analysis. The expressive proteome profiles of HepG2 cells with or without miR-26a mimics treatment were established by the methods of two-dimensional electrophoresis separation following lysis of the cells and extraction of the proteins. The proteomic expression profiles were analyzed by comparative proteomics technique to discover the important protein spots with differential expression. The identification of the proteins was conducted by matrix-assisted laser desorption/ionization time-of-flight mass spectrometry(MALDI-TOF-MS). RESULTS: miR-26a brought down the proliferation of HepG2 cells. Total 11 protein spots with alteration of expressive amounts more than 2 times were successfully identified in the proteomic expression profile of HepG2 cells treated with miR-26a mimics, including annexin A1, peroxiredoxin 4, proliferating cell nuclear antigen, apolipoprotein A1, cytochrome C oxidase subunit 5A, cyclin E2, ribose-phosphate pyrophosphokinase 3, cyclin-dependent kinase 1 and phosphatidylethanolamine-binding protein 1. Among these, the expression of 3 protein spots was up-regulated and 8 of them was down-regulated.CONCLUSION: miR-26a contributes to the anti-cancer effect by expressive regulation of the proteins mentioned above, or directly or indirectly controls the proliferation, differentiation and death of hepatocarcinoma cells.     

Effects of RNA interference of FABP5 on subcutaneous tumor of human hepatocellular carcinoma cell line HepG 2 transplanted in nude mice

AIM: To investigate the effect of recombinant lentiviral vector for RNA interference (RNAi) on the expression of fatty acid-binding protein 5 (FABP5) gene in hepatocellular carcinoma HepG2 cells and tumor formation in nude mice.METHODS: RNAi lentiviral vector was used in the experiment. Human hepatocellular carcinoma HepG2 cells were divided into 3 groups:the HepG2 cells in experimental group were transfected with the recombinant lentivirirus vector LV-shRNA-FABP5, the cells in negative control group were transfected with a control lentiviral vector LV-shRNA-NC, and the cells in normal control group were without any treatment. The nude mice were randomly divided into 3 groups. The growth of the transplanted tumor cells in the nude mice was observed. The tumor growth curve, volume and weight were determined 4 weeks after the cell inoculation. The expression of FABP5 was detected by real-time PCR, Western blot and immunohistochemical staining.RESULTS: Transfection of the lentiviral vector FABP5-shRNA obviously reduced FABP5 expression in the HepG2 cells. Tumor formation was all positive in the 3 groups of the nude mice inoculated with the tumor cells. Compared with normal control group and negative control group, the tumor growth slowed significantly in experimental group with smaller volume and weight. FABP5 expression in the transplanted tumor tissues was significantly down-regulated at mRNA and protein levels in experimental group as compared with normal control group and negative control group.CONCLUSION: RNAi-induced down-regulation of FABP5 effectively inhibits the growth of transplanted hepatocellular carcinoma, suggesting that FABP5 gene may be an effective target for gene therapy in treating liver cancer.