Invasion Of MHCC97H Cells Research Articles

Carnosic acid nanocluster-based framework combined with PD-1 inhibitors impeded tumorigenesis and enhanced immunotherapy in hepatocellular carcinoma.

Clinically, the immune checkpoint inhibitor anti-PD-1 antibody has shown a certain effect in the treatment of hepatocellular carcinoma (HCC), which is limited to a small number of patients with HCC. This study aims to reveal whether carnosic acid nanocluster-based framework (CA-NBF) has a sensitization effect on anti-PD-1 antibody in the treatment of HCC at the cellular and animal levels. MHCC97H cells were treated with CA-NBF, anti-PD-1 and their combination. The effects of CA-NBF and anti-PD-1 on cell proliferation, cell cycle, apoptosis, invasion, and migration were evaluated by MTT assay, flow cytometry, and scratch test. The effects of CA-NBF and anti-PD-1 on Wnt/β-catenin signaling pathway in MHCC97H cells were detected. A BALB/C nude mouse model of hepatocellular carcinoma was established, and the tumor growth was observed at different time points. The expression of cytotoxic T lymphocyte and helper T lymphocyte markers CD8 and CD4 in tumor tissues was detected by immunohistochemistry. Western blotting was used to detect the Wnt/β-catenin signaling pathway proteins (Wnt-3a, β-catenin, and GSK-3β) level in tumor tissues after CA-NBF and anti-PD-1 treatment. CA-NBF activity was significantly higher than CA, which could prominently reduce the proliferation, migration and invasion of MHCC97H cells and enhance apoptosis by inactivating Wnt/β-catenin signaling pathway. CA-NBF combined with anti-PD-1 antibody further enhanced cell proliferation, migration, invasion and pro-apoptosis but had no significant effect on Wnt/β-catenin signaling pathway. CA-NBF in vivo improved the tumor response to PD1 immune checkpoint blockade in HCC, manifested by reducing tumor size and weight, promoting CD4 and CD8 expression. CA-NBF combined with anti-PD-1 have stronger immunomodulatory and anticancer effects without increasing biological toxicity.

Effect of Naringenin on apoptosis and epithelial mesenchymal transition of human high-invasive hepatoma cell line MHCC97-H

Objective To investigate the effect of Naringenin (Nar) on apoptosis, epithelial mesenchymal transition (EMT), of human high-invasive hepatoma cell line MHCC97-H and related molecular mechanisms. Methods MHCC97-H cells were routinely cultured. MTT assay was used to test the effect of Nar on viability of MHCC97-H cells treated with different doses of 0, 40, 80, 160 and 320 μmol/L. Flow cytometry (FCM) was applied to assess the apoptosis rate of MHCC97-H cells treated with Nar. Wound assay and Transwell invasive assay were utilized to assess the EMT of MHCC97-H cells treated with Nar. Real-time quantitative reverse transcriptase-polymerase chain reaction (RT-qPCR) and Western blotting were applied to detect the expression of associated mRNA and proteins with apoptosis and EMT. Results Results of MTT assay showed that decreased cell activity was induced by Nar in a dose-dependent manner. After treatment with 0, 40, 80, 160, 320 μmol/L Nar for 24 h, cell activity was (96.49±13.28)%, (73.65±8.93)%, (60.75±15.75)%, (37.31±7.77)%, and (33.20±10.00)% respectively (F=31.028, P=0.000). After treatment with Nar, apoptosis rate of MHCC97-H cells was increased significantly (t=8.368, P=0.000). Migration and invasion of MHCC97-H cells were decreased after Nar treatment (t=2.964, P=0.014; t=8.899, P=0.000). Results of qPCR and Western blotting demonstrated that associated mRNA and proteins varied after Nar treatment. Conclusion Nar could induce apoptosis and inhibit EMT of MHCC97-H cells. Key words: Liver cancer; Naringenin; Apoptosis; Epithelial mesenchymal transition

The tumor suppressive miR-302c-3p inhibits migration and invasion of hepatocellular carcinoma cells by targeting TRAF4.

MicroRNAs (miRNAs) have been recognized as key regulators of tumorigenesis and progression. Serum miR-302c-3p expression is prominently deregulated in HCV-related hepatocellular carcinoma (HCC). However, the expression of miR-302c-3p and its functional role in HBV-related HCC are rarely investigated. In this study, we found that the expression levels of miR-302c-3p were prominently down-regulated in HCC tissues compared to matched tumor-adjacent tissues. Moreover, miR-302c-3p under-expression was detected in HCC cell lines compared to a normal hepatic cell line LO2. Low miR-302c-3p expression was positively correlated with multiple tumor nodes, venous infiltration and advanced TNM tumor stage of HCC patients. Notably, our follow up data and TCGA data demonstrated that low miR-302c-3p expression predicted a poor survival of HCC patients. Functionally, miR-302c-3p overexpression inhibited migration and invasion of MHCC97H cells in vitro. Additionally, miR-302c-3p knockdown showed an opposite effect on these metastatic behaviors of HepG2 cells. MiR-302c-3p negatively regulated tumor necrosis factor receptor associated factor 4 (TRAF4) abundance by directly targeting 3'-UTR of TRAF4 mRNA. The expression of TRAF4 was up-regulated in HCC tissues. The level of TRAF4 mRNA was inversely correlated with miR-302c-3p expression in HCC specimens. Mechanistically, miR-302c-3p restrained AKT-mediated epithelial-mesenchymal transition (EMT) in HCC cells. Importantly, TRAF4 restoration reversed the inhibitory effect of miR-302c-3p on AKT-induced EMT and HCC cell metastasis. MK2206, an AKT inhibitor, inhibited miR-302c-3p knockdown-induced EMT in HepG2 cells. In summary, these results indicate that miR-302c-3p exhibits a tumor suppressive role in HCC by targeting TRAF4. Inhibition of miR-302c-3p/TRAF4 axis may serve as a therapeutic target for HCC.

MicroRNA-345 inhibits hepatocellular carcinoma metastasis by inhibiting YAP1.

MicroRNAs (miRNAs) play critical roles in hepatocellular carcinoma (HCC). However, the expression and biological function of miR-345 in HCC remain unknown. The present study demonstrated that miR-345 expression was reduced in HCC tissues and cell lines. Decreased miR-345 expression was associated with unfavorable clinical features and poor prognosis. In vitro functional assays showed that miR-345 overexpression inhibited the migration and invasion of MHCC-97H cells while miR-345 knockdown promoted metastatic behavior of Hep3B cells. In vivo experiments showed that miR-345 overexpression inhibited while miR-345 knockdown promoted lung metastasis of HCC cells in nude mice. Mechanically, YAP1 was identified to be the downstream target of miR-345 in HCC cells. YAP1 overexpression reversed the inhibitory effects of miR-345 on MHCC-97H migration and invasion, while YAP1 knockdown reduced the promoting effects of miR-345 knockdown on the metastatic behavior of Hep3B cells.

Effect of recombinant adenovirus harboring snake venom cystatin on invasion and metastasis of human hepatocellular carcinoma cells MHCC97H

Objective To construct recombinant adenovirus harboring snake venom cystatin(Ad/sv-cystatin)and to investigate its effect on invasion and metastasis(in vivo and in vitro)of human hepatocellular carcinoma(HCC)MHCC97Hcells.Methods The recombinant Ad/sv-cystatin harboring sv-cystatin was constructed to infect MHCC97Hcells.Then the growth of MHCC97Hcells was assessed by CCK-8.Transwell matrigel assay was used to assess MHCC97Hcell migration and invasiveness in vitro.Spontaneous lung metastasis assays were used to examine the effects of Ad/sv-cystatin on the invasion and metastasis of MHCC97Hcells invivo.Results Recombinant Ad/sv-cystatin harboring sv-cystatingene could infect MHCC97Hcells.Ad/svcystatin significantly inhibited the growth,migration and invasion of MHCC97Hcells in vitro compared with control and Ad/null groups.Intra-tumoral injection of Ad/sv-cystatin significantly inhibited the lung metastasis of MHCC97Hcells in nude mice compared with control and Ad/null-treated mice.Conclusion It is indicated that recombinant Ad/sv-cystatin can suppress MHCC97Hcell growth,invasion and metastasis in vitro and in vivo,showing apotential for gene therapy of HCC.

Huaier polysaccharides suppresses hepatocarcinoma MHCC97-H cell metastasis via inactivation of EMT and AEG-1 pathway

We have recently reported that astrocyte elevated gene-1 (AEG-1) might be an epithelial–mesenchymal transition (EMT) associated biomarker in human hepatocellular carcinoma (HCC), and play an important role in the progression of hepatocellular carcinoma. To extend our study, we examined here the anti-invasive and metastatic effects of Huaier polysaccharide (HP) on human HCC cell line MHCC97-H and explored its possible mechanism of action. Treatment with HP dose-dependently inhibited the proliferation, adhesion, migration and invasion of MHCC97-H cells in vitro. This was achieved not only by reducing the expression of AEG-1 and N-cadherin, but also by enhancing E-cadherin expression. Therefore, these data suggested that HP can inhibit the growth and metastatic potential of MHCC97-H cells through modulation of the AEG-1/EMT pathway.

Total Flavonoids of Scutellaria barbata Inhibit Invasion of Hepatocarcinoma via MMP/TIMP in Vitro

Metastasis is the major cause of cancer-related deaths. Targeting the process of metastasis has been proposed as a strategy to fight cancer. Scutellaria barbata D. Don (S. barbata), a traditional Chinese medicine, is used for treatment of many diseases, including cancer. This study aimed to determine the anti-metastatic effect of total flavonoids of S. barbata (TF-SB) using the human hepatocarcinoma MHCC97H cell line with high metastatic potential. Our results show that TF-SB could significantly inhibit the proliferation and invasion of MHCC97H cells in a dose-dependent manner. MMP-2 and MMP-9 expression were obviously decreased after TF-SB treatment at both the mRNA and protein level. TIMP-1 and TIMP-2 expression were simultaneously increased. The present study indicates that TF-SB could reduce the metastatic capability of MHCC97H cell, probably through decrease of the MMP expression, and simultaneous increase of the TIMP expression.

Octreotide inhibits proliferation and invasion of MHCC97-H cells in vitro and in vivo

ObjectiveTo figure out the effect of somatostatin analogue Octreotide on proliferation and invasion of human hepatocellular carcinoma cell MHCC97-H and the underlying mechanism in vitro and in vivo. MethodsMHCC97-H cells were treated with Octreotide at the concentration of 0.2 ug/mL in vitro, proliferation related to time was evaluated. After treated with Octreotide at the concentration of 0.2 ug/mL for 48 h, MHCC97-H cells were observed by transmission electron microscope. Cell proliferation was detected by MTT assay after MHCC97-H cells were treated with Octreotide at different concentrations including 0.05, 0.1, 0.2, 0.4, 0.6 and 0.8 ug/mL for 36 h in vitro. 27 nude mice, in which MHCC97-H tumor mass was planted orthotopically, were divided into 3 groups randomly including control group (intraperitoneal injection with equal volume normal saline; n=8), low dose treated group (intraperitoneal injection with Octreotide at 50 ug/kg·d; n=9) and large dose treated group (intraperitoneal injection with Octreotide at 200 ug/kg·d; n=10). All mice were raised for 35 d and sacrificed. The information about survival time, the weight at death point and the pathology change of liver and lung was collected. The expression of vascular endothelial growth factor (VEGF) and matrix metalloproteinases-2 (MMP-2) in mouse HCC tissues were detected by immunohistochemistry finally. ResultsMTT assays showed that Octreotide inhibited the proliferation of MHCC97-H cells significantly. Apoptosis cells were found by transmission electron microscope after treatment with Octreotide at 0.2 ug/mL for 48 h in vitro. The proliferation was inhibited significantly by Octreotide in a dose-dependant manner (r=0.86, P<0.01). Compared with control group, the treated group had the heavier weight at death point and lower intrahepatic metastasis ratio (P<0.05), meanwhile, there was not significant difference in treated groups (P>0.05). The positive expression ratios of VEGF and MMP-2 in treated groups were lower than those in control group (P<0.05), while there was no apparent difference in treated groups (P>0.05). ConclusionOctreotide could inhibit the proliferation of MHCC97-H cells in vitro via inducing apoptosis and the inhibitory function acts in a dose-dependant manner. Octreotide could improve survival of mice with MHCC97-H cells and inhibit the metastasis of MHCC97-H cells in vivo. Regulation of VEGF and MMP-2 expression by Octreotide would be involved in its inhibition in vivo.

A possible connection between adhesion regulating molecule 1 overexpression and nuclear factor kappa B activity in hepatocarcinogenesis

Adhesion regulating molecule 1 (ADRM1), a 19S proteasome cap-associated protein, and nuclear factor kappa B (NF-κB), a protein transcription factor controlling DNA transcription, may play an important role in tumorigenesis. Overexpression of ADRM1 and activation of NF-κB are well-observed in hepatocellular carcinoma (HCC). However, little is known about whether both are functionally connected during hepatocarcinogenesis, and the mechanisms involved. In this study, using laboratory techniques including short hairpin RNA (shRNA)-mediated knockdown, immunohistochemistry (IHC), both semi-quantitative and real-time RT-PCR, western blotting, MTT assay, transwell assay, flow cytometry and electrophoretic mobility shift assay (EMSA), the expression of ADRM1, the effects of ADRM1 knockdown on NF-κB activity, as well as the biological behavior of HCC cells including proliferation, migration, invasion and apoptosis were investigated in the samples from HCC patients and HCC cell lines. We found that both mRNA and protein levels of ADRM1 were increased in HCC tissues and that this increase in ADRM1 expression was parallel to the metastatic potential of HCC cell lines. After ADRM1 knockdown in MHCC97-H cells, the expression of IκB-α was increased and the NF-κB activity was reduced. Furthermore, ADRM1 knockdown inhibited MHCC97-H cell proliferation and induced cell apoptosis, and the migration and invasion of MHCC97-H cells were significantly repressed. These results indicate that there is a clear functional connection between ADRM1 and NF-κB in hepatocarcinogenesis, despite the precise mechanisms through which the two work together still being unknown.

N-terminal and C-terminal heparin-binding domain polypeptides derived from fibronectin reduce adhesion and invasion of liver cancer cells

BackgroundFibronectin (FN) is known to be a large multifunction glycoprotein with binding sites for many substances, including N-terminal and C-terminal heparin-binding domains. We investigated the effects of highly purified rhFNHN29 and rhFNHC36 polypeptides originally cloned from the two heparin-binding domains on the adhesion and invasion of highly metastatic human hepatocellular carcinoma cells (MHCC97H) and analyzed the underlying mechanism involved.MethodsThe MHCC97H cells that adhered to FN in the presence of various concentrations of rhFNHN29 and rhFNHC36 polypeptides were stained with crystal violet and measured, and the effects of rhFNHN29 and rhFNHC36 on the invasion of the MHCC97H cells were then detected using the Matrigel invasion assay as well as a lung-metastasis mouse model. The expression level of integrins and focal adhesion kinase (FAK) phosphotyrosyl protein was examined by Western blot, and the activity of matrix metalloproteinases (MMPs) and activator protein 1 (AP-1) was analyzed by gelatin zymography and the electrophoretic mobility band-shift assay (EMSA), respectively.ResultsBoth of the polypeptides rhFNHN29 and rhFNHC36 inhibited adhesion and invasion of MHCC97H cells; however, rhFNHC36 exhibited inhibition at a lower dose than rhFNHN29. These inhibitory effects were mediated by integrin αvβ3 and reversed by a protein tyrosine phosphatase inhibitor. Polypeptides rhFNHN29 and rhFNHC36 abrogated the tyrosine phosphorylation of focal adhesion kinase (p-FAK) and activation of activator protein 1 (AP-1), resulting in the decrease of integrin αv, β3 and β1 expression as well as the reduction of MMP-9 activity.ConclusionsPolypeptides rhFNHN29 and rhFNHC36 could potentially be applicable to human liver cancer as anti-adhesive and anti-invasive agents.

Human mesenchymal stem cells inhibit metastasis of a hepatocellular carcinoma model using the MHCC97‐H cell line

The effects of mesenchymal stem cells (MSC) on the growth and metastasis of human malignancies including hepatocellular carcinoma (HCC) are controversial, and the underlying mechanisms are not yet understood. The aim of this study was to explore the role of MSC in the progression of HCC. We investigated the effect of MSC on in vitro proliferation and invasion and in vivo tumor growth and pulmonary metastasis of MHCC97-H HCC cells with a high metastatic potential. The mRNA and protein levels of transforming growth factor-beta 1 (TGFβ1) and MMP, and their association with the effects of MSC on HCC cells were also evaluated. Co-culture of MHCC97-H cells with MSC conditioned medium significantly enhanced in vitro proliferation but inhibited invasiveness. Following MSC treatment of a nude mouse model bearing human HCC, the MSC were predominantly located in the HCC tissues. Compared with controls, MSC-treated mice exhibited significantly larger tumors (3080.51 ± 1234.78 mm(3) vs 2223.75 ± 1000.60 mm(3), P = 0.045), but decreased cellular numbers of lung metastases (49.75 ± 18.86 vs 227.22 ± 74.67, P = 0.046). Expression of TGFβ1 and MMP-2 was significantly downregulated in the MSC-treated HCC cells. TGFβ siRNA concurrently downregulated expression of TGFβ and MMP-2 in HCC cells and blocked the MSC-induced proliferation and invasiveness of MHCC97-H cells. The MSC enhanced tumor growth but significantly inhibited the invasiveness and metastasis of HCC, possibly through downregulation of TGFβ1. These findings suggest that MSC could be useful in controlling metastatic recurrence of HCC.

Chrysanthemum indicum ethanolic extract inhibits invasion of hepatocellular carcinoma via regulation of MMP/TIMP balance as therapeutic target

Hepatocellular carcinoma (HCC) is an aggressive cancer with a dismal outcome largely due to metastasis and postsurgical recurrence. Thus, the inhibition of invasion and metastasis is of great importance in its therapies. Medicinal plants or ethnopharmacology used in folklore medicine continue to be an important source of discovery and development of novel or potential therapeutic agents for treatment of cancer. Chrysanthemum indicum, one of the medicinal plants or ethnopharmacology, is being used for treatment of many diseases including cancer. However, this plant molecular mechanisms underlining the anti-metastatic effects have not been well documented. In this study, Chrysanthemum indicum ethanolic extract (CIE) significantly suppressed proliferation and invasion of MHCC97H cells, one of the HCC cell lines with high metastatic potential, in a dose-dependent manner. CIE markedly decreased MMP-2 and MMP-9 expression, increased simultaneously TIMP-1, and TIMP-2 expression further restoring their balance in the cancer cells. The present study indicates that CIE reduced MHCC97H cell metastatic capability, in part at least, through decrease of the MMP expression, simultaneous increase of the TIMP expression, further restoring their balance as therapeutic target in HCC. It is suggested that Chrysanthemum indicum is a potential novel therapeutic medicinal plant for treatment of HCC or cancer invasion and metastasis.

Inhibitory effect of anti-hepatitis drug bicyclol on invasion of human hepatocellular carcinoma MHCC97-H cells with high metastasis potential and its relative mechanisms

To assess the anti-invasion effect of bicyclol (1) and its mechanism in human hepatocellular carcinoma (HCC) MHCC97-H cells with high metastatic potential. MTT assay was performed to evaluate the cytotoxicity of 1 to MHCC97-H cells and its inhibitory effect on the adhesion of these cells to laminin (LN) and fibronectin (FN). The anti-invasion effect of 1 was detected in an experiment using a transwell chamber. Transcription of vascular endothelial growth factor (VEGF), nm23-H1, and urokinase-type plasminogen activator receptor (uPAR) mRNAs was determined by an RT-PCR assay. The secretion and expression of α-fetoprotein (AFP) were analyzed by ELISA and flow cytometry, respectively. At concentrations of 10, 50, and 100 μmol/l, 1 obviously inhibited the adhesion of the MHCC97-H cells to LN and FN. The rates of inhibition of MHCC97-H cell invasion by 50 and 100 μmol/l for 1 were 37.3 and 50.2%, respectively. Drug 1 also decreased the expressions of VEGF, nm23-H1, and uPAR mRNA and the secretion of AFP in MHCC97-H cells. At low cytotoxic concentrations, the anti-hepatitis drug 1 demonstrated a significant anti-invasive effect in human HCC MHCC97-H cells with high metastatic potential. The inhibition of the expressions of VEGF, nm23-H1, and uPAR should contribute, at least in part, to the anti-invasion property of 1.

Down-Regulation of c-Met Expression Inhibits Human HCC Cells Growth and Invasion by RNA Interference

Cell migration is a basis for invasion and metastasis of malignant tumors. Receptor tyrosine kinases are recognized as important therapeutic targets in antineoplastic strategies. C-met is a receptor tyrosine kinase highly expressed in human hepatocellular carcinoma (HCC) cell line MHCC97-H. Higher expression of c-met in tumor tissue can lead to scattering, angiogenesis, proliferation, enhanced cell motility, invasion, and eventually, metastasis. To explore the roles of c-met in modulating the motility of cell, we silenced c-met expression in the HCC line MHCC97-H by RNA interference (RNAi). For transient expression, c-met-siRNA 1,2 recombinant plasmids were transfected into phoenix A cells. The MHCC97-H cells were cultured in Dulbecco's modified Eagles's medium (DMEM) with 10% fetal bovine serum (FBS) to establish MHCC97-H HCC cells stably expressing c-met-siRNA. MHCC97-H cells were treated with the recombinant virus for assay of c-met mRNA and protein, evaluation of growth and invasion of MHCC97-H cells, and identification of hepatitis B virus X (HBX) protein correlation with c-met. After transfection of c-met-siRNA for 48 h, the expression of c-met decreased markedly in MHCC97-H cells; the most effective site of the siRNA target sequence is at the 537 upstream, far from the transcription start. In addition, the proliferation, motility, and invasive ability of MHCC97-H cells were significantly inhibited. Furthermore, we showed that hepatitis B virus (HBV) X protein (HBX) potentiated the activities of the extracellular signal-regulated kinase 1/2 (ERK1/2) in MHCC97-H cells. Treatment with extracellular signal-regulated kinase (ERK) inhibitor (U0126), but not P38 MAPK inhibitor (SB203580) or phosphatidylinositol 3-kinase (PI3K) inhibitor (wortmannin), markedly suppressed the expression of c-met protein in MHCC97-H cells. These results indicate that the over-expression of c-met protein plays an important role in the cell invasion of MHCC97-H, and HBX protein may promote the expression of c-met by ERKs pathway.

Inhibitory effects of genistein on metastasis of human hepatocellular carcinoma

To investigate the inhibitory effects of genistein on metastasis of MHCC97-H hepatocellular carcinoma cells and to explore the underlying mechanism. MHCC97-H hepatocellular carcinoma cells were exposed to genistein. A cell attachment assay was carried out in a microculture well pre-coated with fibronectin. The invasive activity of tumor cells was assayed in a transwell cell culture chamber, and cell cycle and apoptosis were evaluated by a functional assay. In addition, the expression and phosphorylation of FAK were detected by Western blotting. In situ xenograft transplantation of hepatocellular carcinoma was performed in 12 nude mice and lung metastasis of hepatocellular carcinoma was observed. Genistein significantly inhibited the growth of MHCC97-H cells in vitro. Adhesion and invasiveness of MHCC97-H cells were inhibited in a concentration-dependent fashion, and the inhibitory effect of genistein was more potent in the 10 microg/mL and 20 microg/mL genistein-treated groups. Genistein caused G(0)/G(1) cell cycle arrest, an S phase decrease, and increased apoptosis. The expression and phosphorylation of FAK in MHCC-97H cells were significantly decreased. In situ xenograft transplantation of hepatocellular carcinoma was also significantly suppressed by genistein. The number of pulmonary micrometastatic foci in the genistein group was significantly lower compared with the control group (12.3 +/- 1.8 vs 16.6 +/- 2.6, P < 0.05). Genistein appears to be a promising agent in the inhibition of metastasis of hepatocellular carcinoma.

Role of focal adhesion kinase in induction of adhesion and invasion of MHCC-97H cells by PDGF-BB

目的 观察不同浓度血小板衍生生长因子(PDGF-BB)诱导MHCC-97H细胞中粘着斑激酶(focal adhesion kinase,FAK)mRNA的动态变化及FAK在细胞黏附、侵袭的作用.方法 不同浓度(1,2.5,5,10,25ng/ml)PDGF-BB诱导MHCC-97H人肝癌细胞,Real-time PCR方法检测FAK及MMP-2的mRNA动态变化,黏附实验、侵袭实验分别检测诱导后MHCC-97H细胞的黏附、侵袭能力的变化.结果 诱导后MHCC-97H细胞FAK mRNA水平上调,在10ng/ml浓度时达到最高,为对照组的112.6倍;MMP-2mRNA水平上调并与FAK mRNA水平上调呈一致性,在10ng/ml浓度时达到最高,为对照组的56.9倍.诱导后各组黏附率分别为(66±1.84)%、(69±1.41)%、(69±2.42)%、(71±1.37)%和(66±3.28)%,与对照组的(54±2.08)%比较均有统计学意义(P＜0.001);诱导后5ng/ml和10ng/ml组侵袭细胞数分别为(26.63±4.5)、(28.75±4.2)个,与对照组(21.5±4.0)个比较有显著性差异(P＜0.05,P%0.001).诱导后黏附率与侵袭细胞数变化在10ng/ml浓度时都达到高峰.结论 PDGF-BB上调MHCC-97H细胞中FAK表达,上调FAK促进MHCC-97H细胞的黏附和侵袭能力。