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1.
AIM:To investigate the effects of luteolin on the invasion and epithelial-mesenchymal transition (EMT) induced by transforming growth factor-β1 (TGF-β1) in lung cancer A549 cells. METHODS:The effect of luteolin at 5, 10, 20, 40, 80 and 160 μmol/L on the viability of A549 cells was measured by MTT assay. The invasion ability was analyzed by Transwell method. The morphological changes of the A549 cells were observed under microscope.The protein expression of E-cadherin and vimentin in the A549 cells were determined by Western blot. RESULTS:The viability of the A549 cells was significantly inhibited by luteolin in a dose-time dependent manner (P<0.05). The IC50 of luteolin for the A549 cells (24 h) was 68.79 μmol/L, while that (48 h) was 47.86 μmol/L. TGF-β1 induced morphological alteration of the A549 cells from epithelial to mesenchymal forms. Luteolin significantly inhibited TGF-β1-induced invasion of the A549 cells (P<0.01). The protein expression of E-cadherin was significantly down-regulated and the protein expression of vimentin was significantly up-regulated in the presence of TGF-β1 at 5 μg/L (P<0.01). However, luteolin reversed TGF-β1-induced EMT, up-regulation of E-cadherin and down-regulation of vimentin (P<0.01). CONCLUSION:Lu-teolin reverses TGF-β1-induced EMT in the lung cancer A549 cells.  相似文献   

2.
SHEN Dong  WANG Wei 《园艺学报》2018,34(9):1622-1626
AIM:To investigate the effects of shikonin on the migration, invasion and epithelial-mesenchymal transition (EMT) in human non-small-cell lung cancer PC9 cells induced by hepatocyte growth factor (HGF). METHODS:The effect of shikonin on the viability of PC9 cells was measured by MTT assay. The cell migration and invasion abilities were analyzed by wound healing assay and Transwell method, respectively. The protein expression levels of E-cadherin, N-cadherin and vimentin in the PC9 cells were determined by Western blot. RESULTS:The viability of PC9 cells was significantly inhibited by shikonin in a dose-dependent manner (P<0.01), with IC50 at 9.364 μmol/L. HGF significantly promoted the abilities of migration and invasion, and induced EMT in the PC9 cells. Shikonin significantly inhibited HGF-induced migration and invasion in the PC9 cells. The expression of E-cadherin was significantly down-regulated and the expression of N-cadherin and vimentin was significantly up-regulated in the presence of HGF (50 μg/L). However, shikonin reversed HGF-induced EMT, as indicated by up-regulation of E-cadherin and down-regulation of N-cadherin and vimentin (P<0.01). CONCLUSION:Shikonin reverses HGF-induced EMT in lung cancer PC9 cells.  相似文献   

3.
AIM: To investigate the mechanism of microRNA-138-5p (miR-138-5p) inhibiting the proliferation, migration and invasion abilities of lung cancer cells.METHODS: The lung cancer A549 and H460 cells were transfected with miR-NC (control group) or miR-138-5p (experimental group). The bioinformatic analysis was performed to predict the target genes of miR-138-5p.The expression levels of miR-138-5p, forkhead box protein C1 (FOXC1) mRNA and vimentin mRNA were detected by RT-qPCR. The protein expression of FOXC1, vimentin, E-cadherin, N-cadherin and β-catenin was determined by Western blot. MTS method and colony formation assay were used to detect cell viability and proliferation ability. Wound healing assay and Transwell assay were used to detect cell migration and invasion ability.RESULTS: Over-expression of miR-138-5p significantly reduced the expression of FOXC1 and vimentin at mRNA and protein levels (P<0.05). The expression of E-cadherin and β-catenin were up-regulated and the expression of N-cadherin was down-regulated. The proliferation, migration and invasion abilities of the lung cancer cells were inhibited by the over-expression of miR-138-5p.CONCLUSION: miR-138-5p inhibits the proliferation, migration and invasion abilities of lung cancer cells by targeting FOXC1 and vimentin. It may be a potential target for lung cancer gene therapy.  相似文献   

4.
AIM: To explore the inhibitory effects of pantoprazole sodium on epithelial-mesenchymal transition and cisplatin resistance in lung cancer cells and the underlying mechanism.METHODS: Using MTT method, wound healing assay, Transwell experiment, Western blot, the differences of morphology, invasion ability, migration ability, drug sensitivity and protein expression between A549/DDP cells and A549 cells were determined. The effect of pantoprazole sodium on morphology, invasion ability, migration ability, drug sensitivity and protein expression in A549/DDP cells were also observed.RESULTS: Compared with A549 cells, A549/DDP cells had higher invasion and migration abilities, and lower drug sensitivity, exhibited mesenchymal phenotype and activated c-Met/AKT/mTOR pathway. Pantoprazole sodium inhibited the abilities of invasion and migration, and reversed the mesenchymal phenotype, drug resistance and the c-Met/AKT/mTOR pathway activation in A549/DDP cells. Treatment with c-Met inhibitor SU11274, PI3K inhibitor LY294002 and mTOR inhibitor rapamycin had the same effects on A549/DDP cells as that of pantoprazole sodium.CONCLUSION: Pantoprazole sodium inhibits invasion, migration, epithelial-mesenchymal transition and cisplatin resistance in lung cancer cells by down-regulating c-Met/AKT/mTOR pathways.  相似文献   

5.
LI Bai-he  YUAN Lei 《园艺学报》2016,32(5):852-856
AIM: To investigate the effect of digoxin on hypoxia-induced epithelial-mesenchymal transition (EMT), migration and invasion in human breast carcinoma MCF-7 cells. METHODS: MCF-7 cells were treated in vitro with a chemical hypoxia inducer cobalt chloride (CoCl2) to imitate hypoxia. Cell migration was observed by wound healing assay, and cell invasion was measured by Transwell invasion assay. The protein levels of hypoxia-inducible factor-1α (HIF-1α), Snail, E-cadherin and vimentin in MCF-7 cells were detected by Western blot. RESULTS: Digoxin inhibited CoCl2-induced EMT and reversed the mesenchymal phenotype. CoCl2 enhanced the abilities of migration and invasion (P<0.01), significantly decreased the expression of E-cadherin and increased the expression of HIF-1α, Snail and vimentin (P<0.01), but these effects were blocked by digoxin. CONCLUSION: Digoxin inhibits CoCl2-induced EMT and invasion most likely via HIF1-α-Snail signaling pathway.  相似文献   

6.
AIM: To investigate the effects of microRNA(miRNA)-126 on the proliferation, migration and invasion of human lung cancer cell lines, and to explore its mechanism. METHODS: The A549 cells were transfected with miRNA-126 agomir by Lipofectamine 2000. The expression of miRNA-126 was detected by real-time PCR. The cell activity was detected by MTT assay. The number of viable A549 cells was counted by the method of Trypan blue exclusion. The cell colony-forming capability was determined by cell colony formation test. The cell migration and invasion abilities were assayed by wound healing and Transwell methods, respectively. The protein levels of p-EGFR, EGFR, p-AKT, AKT, p-mTOR and mTOR were determined by Western blot. RESULTS: The expression level of miRNA-126 was significantly increased in the A549 cells compared with negative control(NC) group and control group(P<0.01). The proliferation of A549 cells was decreased extremely after transfected with the miRNA-126 agomir(P<0.01), so did the result of the cell colony-formation test. The migration and invasion abilities of the lung cancer cells were also significantly inhibited. The protein levels of p-EGFR, p-AKT and p-mTOR were significantly down-regulated compared with NC group and control group(P<0.01). CONCLUSION: Over-expression of miRNA-126 significantly inhibits the proliferation, migration and invasion ability of human lung cancer A549 cells by down-regulation of EGFR/AKT/mTOR pathway.  相似文献   

7.
AIM: To investigate the function of microRNA-125a-5p (miR-125a-5p) on epithelial-mesenchymal transition (EMT) of breast cancer cells via GSK-3β/Snail signaling pathway.METHODS: The expression of miR-125a-5p in normal breast epithelial cells and breast cancer cells, as well as the transfection efficiency of miR-125a-5p plasmid in MDA-MB-231 cells was detected by RT-qPCR. The chemotaxis ability and invasion ability were detected by chemotaxis assay and Transwell invasion assay. The changes of EMT-related markers, the protein level of phosphorylated glycogen synthase kinase-3β (p-GSK-3β) and the nuclear translocation of Snail were determined by Western blot. RESULTS: The expression of miR-125a-5p in the breast cancer cells was significantly lower than that in the normal breast epithelial cells. The expression of miR-125a-5p was significantly higher in MDA-MB-231/miR-125a-5p cells than that in MDA-MB-231/NC cells. The ability of epithelial growth factor (EGF) at 10 μg/L to induce chemotaxis of MDA-MB-231 cells was the strongest. Compared with MDA-MB-231/NC group, stimulation of EGF decreased the invasion ability of MDA-MB-231/miR-125a-5p cells, and resulted in the increase in E-cadherin expression, while significantly decreased the protein levels of vimentin and p-GSK-3β. Meanwhile, the nuclear localization of Snail was significantly inhibited. The invasion capacity of MDA-MB-231/miR-125a-5p+GAB2 cells was significantly enhanced compared with MDA-MB-231/miR-125a-5p+Con cells, the expression of E-cadherin was decreased, and the protein levels of vimentin and p-GSK-3β were significantly increased, while the nuclear localization of Snail was promoted. CONCLUSION: miR-125a-5p suppresses EMT via GSK-3β/Snail signaling pathway, thus inhibiting the invasion ability of breast cancer cells.  相似文献   

8.
AIM To explore the molecular mechanism of transforming growth factor-β1 （TGF-β1）-induced epithelial-mesenchymal transition （EMT） and cisplatin resistance in three-dimensionally cultured lung cancer cells. METHODS Under three-dimensional culture condition, the morphological changes and protein expression changes of human non-small-cell lung cancer 95D cells were observed by inversed fluorescence microscopy, scanning electron microscopy, laser scanning confocal microscopy and Western blot before or after TGF-β1 stimulation. The cisplatin sensitivity was determined by MTT assay. RESULTS Under the three-dimensional culture condition, the structure of 95D cell spheroids after TGF-β1 stimulation collapsed, the cells were dispersed and migrating, and the spheroids merged with each other. The results of laser confocal microscopy showed that E-cadherin protein expression in the 95D cells did not changed after TGF-β1 stimulation, and the protein expression of N-cadherin and vimentin was significantly up-regulated. The results of Western blot showed that the expression of E-cadherin was down-regulated after TGF-β1 stimulation, and the protein levels of N-cadherin, vimentin, phosphorylated AKT and phosphorylated mTOR were up-regulated. LY294002 and rapamycin reversed TGF-β1-induced expression of the above proteins. The results of MTT assay showed that TGF-β1 reduced the sensitivity of three-dimensionally cultured 95D cells to cisplatin, while LY294002 and rapamycin reversed the cisplatin resistance of the 95D cells stimulated by TGF-β1. CONCLUSION TGF-β1 induces the EMT and cisplatin resistance of three-dimensionally cultured lung cancer cells through the activation of PI3K/AKT/mTOR signaling pathway.  相似文献   

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11.
AIM: To explore the effect of new artificially synthesized androgen receptor (AR) antagonist HC-1119 on the biological function of triple-negative breast cancer (TNBC) BT549 cells and the molecular mechanism. METHODS: The AR expression was assessed in different human breast cancer cell lines MDA-MB-231, T47D, MCF-7, SKBR3 and BT549 by Western blot. The TNBC BT549 cells with AR positive expression were treated with HC-1119. The cell viability was measured by CCK-8 assay. The apoptosis rate and cell cycle distribution were analyzed by flow cytometry. The migration and invasion abilities were detected by Transwell assay in vitro. The protein expression of E-cadherin, vimentin and P21 was determined by Western blot. RESULTS: AR was positively expressed in BT549 cells. HC-1119 inhibited the cell viability in a time-and dose-dependent manner (P<0.05), increased the percentage of apoptotic cells and the percentage of S-phase cells significantly, repressed the migration and invasion abilities (P<0.05), and decreased P21 expression at protein level (P<0.01). No influence on the expression of E-cadherin and vimentin in the BT549 cells was observed. CONCLUSION: AR antagonist HC-1119 decreases the viability, migration ability and invasion ability, enhances the apoptosis, and arrests the cell cycle distribution of TNBC BT549 cells. HC-1119 represses the viability of BT549 cells by down-regulating P21 expression, while the process of epithelial-mesenchymal transition is not involved in the inhibition of cell migration.  相似文献   

12.
YU Dan  LIU Xia  FAN Wan-lin  AN Xiang  LI Bing 《园艺学报》2018,34(7):1250-1255
AIM:To investigate the effect of X-ray ionizing radiation on epithelial-mesenchymal transition (EMT) in human nasopharyngeal carcinoma CNE-2 cells and its involved potential signaling pathway. METHODS:The nasopharyngeal carcinoma CNE-2 cells were irradiated with different doses (0 Gy, 2 Gy, 4 Gy and 8 Gy) of X-ray. The morphological changes of the cells were observed under inverted microscope after 24 h. The migration and invasion abilities were detected by wound healing and Transwell assays. The mRNA and protein levels of E-cadherin, N-cadherin and vimentin in nasopharyngeal carcinoma CNE-2 cells were determined by real-time PCR and Western blot, respectively. The protein levels of Akt and p-Akt were detected by Western blot. RESULTS:After X-ray irradiation, the CNE-2 cells exhibited typical ‘cobblestone’ or spindle-like shape, with extended pseudopodia and dilated intercellular space. The invasiveness and metastatic abilities of the CNE-2 cells were enhanced (P<0.01). The mRNA and protein expression levels of E-cadherin were significantly decreased (P<0.01), while the mRNA and protein expression levels of N-cadherin and vimentin were markedly increased after irradiation as compared with the control group (no irradiation) (P<0.05). The protein level of p-Akt was significantly enhanced (P<0.01), while the protein level of Akt showed little change after irradiation. CONCLUSION:X-ray ionizing radiation induces EMT in nasopharyngeal carcinoma CNE-2 cells, which may be related to the activation of PI3K/Akt signaling pathway.  相似文献   

13.
AIM: To investigate the effect of Eph receptor A2 (EphA2) on drug resistance of colorectal carcinoma cells and its possible mechanisms. METHODS: Real-time PCR and Western blot were used to detect the expression of EphA2 at mRNA and protein levels in LoVo and LoVo/5-FU cells. EphA2 siRNA was transfected to down-regulate the EphA2 expression in LoVo/5-FU cells, and the drug sensitivity was calculated by CCK-8 assay. Meanwhile, cell migration and invasion were measured by wound healing assay and Transwell assay, and the protein levels of E-cadherin, β-catenin, N-cadherin, vimentin, Notch and Snail were determined by Western blot. RESULTS: The expression of EphA2 at both mRNA and protein levels was significantly up-regulated in LoVo/5-FU cells (P<0.05). Knockdown of EphA2 suppressed the cell viability, and migration and invasion abilities, but promoted drug sensitivity of LoVo/5-FU cells. Up-regulation of E-cadherin and β-catenin, and down-regulation of N-cadherin and vimentin were observed, indicating that the epithelial-mesenchymal transition (EMT) process was suppressed. Knockdown of EphA2 decreased the expression levels of Notch and Snail. CONCLUSION: Down-regulation of EphA2 partly reverses drug resistance of LoVo/5-FU cells. The mechanism may be related to suppressing cell growth, migration, invasion and EMT process via Notch/Snail signaling pathway.  相似文献   

14.
AIM:To investigate the effect of interleukin-6 (IL-6) on epithelial-mesenchymal transition (EMT), migration and invasion of papillary thyroid carcinoma TPC-1 cells by inducing the expression of long noncoding RNA lncTCF7. METHODS:The effects of IL-6 on the expression of lncTCF7 in the TPC-1 cells were detected by RT-qPCR after the TPC-1 cells were treated with IL-6 at 0, 5, 10, 20 and 50 μg/L for 24 h or with IL-6 at 50 μg/L for 0, 6, 12 and 24 h. After the TPC-1 cells were treated with IL-6 at 50 μg/L for 24 h, the effect of IL-6 on the protein expression of E-cadherin and vimentin in the TPC-1 cells was detected by Western blot. The TPC-1 cell line with lncTCF7 over-expression was established, and the effects of lncTCF7 over-expression on EMT, migration and invasion of the TPC-1 cells were measured by Western blot and Transwell assay. After knockdown of lncTCF7 expression and exposure to IL-6 at 50 μg/L, the effects of lncTCF7 on EMT, migration and invasion of TPC-1 cells treated with IL-6 were observed. RESULTS:The expression of lncTCF7 in the TPC-1 cells was induced by IL-6 in a dose-and time-dependent manner. The expression of E-cadherin was down-regulated, the expression of vimentin was up-regulated, and the migration and invasion abilities of the TPC-1 cells were enhanced by lncTCF7 over-expression (P<0.05). The expression of E-cadherin was decreased, the expression of vimentin, Snail and Slug was increased, and the migration and invasion abilities of the TPC-1 cells and intercellular space were enhanced by IL-6. The above changes induced by IL-6 were significantly inhibited by knockdown of lncTCF7 expression. CONCLUSION:IL-6 promotes the EMT, migration and invasion of papillary thyroid carcinoma TPC-1 cells by inducing the expression of lncTCF7.  相似文献   

15.
AIM: To investigate the molecular mechanism of polypyrimidine tract-binding protein 1 (PTBP1) promoting the migration and invasion of hepatoma cells. METHODS: The differentially expressed splicing proteins in different cell lines were screened by qPCR and Western blot. The difference of the expression of PTBP1 between liver cancer and normal liver tissues was analyzed by bioinformatics. Wound-healing and Transwell assays were used to study the effect of PTBP1 on the migration and invasion of hepatoma cells, and Western blot was used to detect the effect of PTBP1 on epithelial-mesenchymal transition (EMT) signaling pathway. RESULTS: Compared with the HepG2 cells, the expression of splicing factor PTBP1 was significantly increased in the HCCLM3 cells with high metastatic ability (P<0.05), and the expression level of PTBP1 in hepatocellular carcinoma tissues was significantly higher than that in normal tissues (P<0.05). Over-expression of PTBP1 significantly increased the migration and invasion of HCCLM3 cells (P<0.05), increased the expression of mesenchymal marker proteins N-cadherin and vimentin (P<0.05), and promoted the EMT process of liver cancer cells. CONCLUSION: PTBP1 promotes the migration and invasion of liver cancer cells by promoting the EMT pathway of liver cancer cells.  相似文献   

16.
AIM: To investigate the effect of toosendanin (TSN) on invasion and migration abilities of human ovarian cancer cells and the related mechanism. METHODS: The human ovarian cancer cell lines CAVO-3 and SKVO-3 were treated with TSN at different concentrations. The cell viabilty at 12, 24, 48, 72 and 96 h after TSN treatment was measured by CCK-8 assay. Scratch wound healing assay and Transwell assay were employed to measure the invasion and migration abilities of CAVO-3 cells. The protein expression of nuclear factor-κB (NF-κB) p65, E-cadherin, N-cadherin, vimentin and Snail was determined by Western blot. RESULTS: TSN significantly inhibited the viability of CAVO-3 and SKVO-3 cells (P<0.05). Compared with control group, the migration and invasion abilities of CAVO-3 cells in TSN group decreased significantly (P<0.05). In addition, the expression of NF-κB p65 and E-cadherin protein increased notably, followed with N-cadherin, vimentin and Snail protein decreased significantly (P<0.05). However, the inhibitor of NF-κB BAY11-7082 reversed the impact above. Compared with TSN group, the migration and invasion abilities in TSN+BAY11-7082 group increased significantly (P<0.05). The protein expression of E-cadherin also decreased notably, followed with the protein expression of N-cadherin, vimentin and Snail increased significantly (P<0.05). CONCLUSION: TSN inhibits the invasion and migration abilities of human ovarian cancer cells, which is related to the inhibition of epithelial-mesenchymal transition process mediated by NF-κB/Snail signaling pathway.  相似文献   

17.
LIANG Min  CHEN Xin 《园艺学报》2016,32(12):2239-2244
AIM: To investigate the effects of ursolic acid (UA) on the migration and invasion of human lung cancer cell line A549, and to explore its mechanism. METHODS: The cell viability was detected by MTT assay. The expression of miRNA-133a was detected in the A549 cells treated with UA by real-time PCR. The miRNA-133a mimics and inhibitor were transfected into the A549 cells, and the transfection efficiency was analyzed by real-time PCR. The cell migratory and invasive abilities were determined by wound healing and Transwell methods, respectively. RESULTS: The viability of the human lung cancer A549 cells was significantly inhibited by UA in a dose-dependent manner (P<0.05). IC50 of UA (24 h) for lung cancer A549 cells was 31.04 μmol/L. UA treatment significantly inhibited the migratory and invasive abilities of A549 cells in a concentration-dependent manner, accompanied by significantly elevation of miRNA-133a expression. The mimics and inhibitor of miRNA-133a significantly upregulated and downregulated the expression of miRNA-133a in the transfected A549 cells, respectively. In addition, the viability of the A549 cells was decreased extremely after tansfected with the miRNA-133a mimics (P<0.01), so did the results of the cell migration and invasion test. The A549 cells tansfected with the miRNA-133a inhibitor showed an opposite changes of the cell viability, migration and invasion. CONCLUSION: UA inhibited the viability, migration and invasion of lung cancer A549 cells by elevating the expression of miRNA-133a.  相似文献   

18.
AIM: To explore the target relationship between microRNA-140-3p (miR-140-3p) and programmed cell death ligand 1 (PD-L1) and their effect on the viability, migration and invasion of non-small-cell lung cancer A549 cells.METHODS: RT-qPCR was used to detect the miR-140-3p expression in HLF-1, A549 and H1299 cells, and then the A549 cells with the most significant difference were selected as the subsequent research object. TargetScan software and dual-luciferase reporter assay were performed to predict and confirm the target relationship between miR-140-3p and PD-L1. RT-qPCR and Western blot were used to determine the effects of miR-140-3p mimic and inhibitor on PD-L1 expression level. MTT assay was used to detect the viability of A549 cells. Transwell assay was performed to detect the migration and invasion abilities of the A549 cells.RESULTS: miR-140-3p was significantly down-regulated in the A549 cells and H1299 cells (P<0.05). Transfection with miR-140-3p mimic decreased the expression of PD-L1 and inhibited the viability, migration and invasion of the A549 cells. Transfection with pcDNA3.0-PD-L1 reversed the inhibitory effect of miR-140-3p on the viability, migration and invasion of the A549 cells.CONCLUSION: miR-140-3p inhibits the viability, migration and invasion of A549 cells by targeting PD-L1.  相似文献   

19.
AIM To explore the expression of perilipin 3（PLIN3） in lung adenocarcinoma and the relationship between the prognosis of patients and the invasiveness of lung adenocarcinoma cells. METHODS HPA database was used to predict the genes related to poor prognosis of lung cancer and PLIN3 was selected as the research object.HPA database was used to analyze the correlation between PLIN3 and survival rate of lung cancer and lung adenocarcinoma.GEPIA database was used to further verify the correlation between the expression difference of PLIN3 and the survival rate of lung adenocarcinoma patients. The expression of PLIN3 in lung adenocarcinoma was further analyzed by using Ualcan database.Western blot was used to detect the expression of PLIN3 in lung adenocarcinoma cells.siPLIN3 plasmid was constructured and Transwell assay was used to detect the invasion ability of A549 cells after transfection. RESULTS PLIN3 was significantly related to the survival rate of the patients with lung adenocarcinoma and it was over-expressed in lung adenocarcinoma tissues.The expression of PLIN3 was closely related to the stages of cancer and the grades of lymph node metastasis of lung adenocarcinoma.PLIN3 was over-expressed in lung adenocarcinoma cells. The number of the A549 cells passing through Transwell in knock-down group was significantly lower than that in control group. CONCLUSION PLIN3 is highly expressed in lung adenocarcinoma. The expression level of PLIN3 is related to the prognosis of lung adenocarcinoma patients.Knock-down of PLIN3 inhibits the invasion ability of lung adenocarcinoma cells in vitro.  相似文献   

20.
SUN Jie  FU Li-fang 《园艺学报》2017,33(8):1428-1435
AIM: To explore the expression of Dickkopf-1 (DKK1) in human gastric carcinoma cells, and the influences of DKK1 gene silencing on cell invasion. METHODS: The levels of DKK1 in the human gastric mucosa cell line GES-1 and gastric carcinoma cell lines MKN-45 and SGC-7901 were detected by real-time PCR and Western blot. DKK1 gene was silenced by RNA interference, which was verified by real-time PCR, Western blot and ELISA. The cell invasion ability was determined by Transwell assay, and the cell proliferation was inhibited by mitomycin C. The levels of E-cadherin, N-cadherin, vimentin and β-catenin were determined by real-time PCR and Western blot. RESULTS: The expression of DKK1 was significantly higher in MKN-45 cells and SGC-7901 cells than that in GES-1 cells, indicating that DKK1 expression was obviously increased in gastric carcinoma cells. After successful silencing of DKK1 gene in the MKN-45 cells and SGC-7901 cells, the cell invasion ability was markedly decreased in a time-dependent pattern with increased expression of E-cadherin and decreased expression of N-cadherin and vimentin, indicating that DKK1 silencing dramatically inhibited gastric carcinoma cell invasion and epithelial-mesenchymal transition (EMT). The introduction of exogenous recombinant DKK1 (rDKK1) demonstrated the promoting effect of DKK1 on gastric carcinoma cell invasion and EMT. In addition, the inhibitory effects of DKK1 silencing on gastric carcinoma cell invasion and EMT were fulfilled by down-regulating β-catenin. CONCLUSION: The expression of DKK1 is significantly increased in human gastric carcinoma cells. Silencing of DKK1 markedly inhibits gastric carcinoma cell invasion and EMT by down-regulating β-catenin.  相似文献   

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