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Objective To investigate the effects on cell proliferation and invasion of the circular RNA hsa_circ_0067582 in gastric cancer(GC). Methods After hsa_circ_0067582 overexpression (Oe-circ_0067582) plasmid was transfected into AGS and SGC-7901 cells,the cell viability,proliferation,invasion ability,and apoptosis were detected by CCK-8,colony formation and EdU assays,Transwell assay,and flow cytometry,respectively.Western blotting was employed to detect the expression levels of proteins related to the cell apoptosis and epithelial-mesenchymal transition(EMT).The effect of Oe-circ_0067582 on the growth of SGC-7901 cells in nude mice was observed.Bioinformatics tools were used to predict the binding target miRNA of hsa_circ_0067582,and the competing endogenous RNA(ceRNA)regulatory network was established.Finally,functional enrichment was performed to analyze the biological functions of the target genes of the predicted miRNA. Results Compared with the pLO-ciR(empty plasmid)group,the Oe-circ_0067582 group in AGS and SGC-7901 cells attenuated the cell viability(t=7.883,P=0.001;t=5.679,P=0.005),proliferation(t=6.709,P=0.003;t=5.857,P=0.003),and invasion ability(t=7.782,P=0.002;t=6.342,P=0.003)and induced cell apoptosis(t=7.225,P=0.002;t=11.509,P=0.001).Western blotting showed that the Oe-circ_0067582 group in AGS and SGC-7901 cells up-regulated the protein levels of cysteinyl aspartate specific proteinase (Caspase) 3(t=6.863,P=0.002;t=7.024,P=0.001),Caspase 7(t=3.295,P=0.04;t=6.008,P=0.004),Caspase 9(t=4.408,P=0.012;t=6.278,P=0.004),and E-cadherin(t=12.453,P=0.002;t=10.867,P=0.001),while down-regulated those of Vimentin(t=7.242,P=0.002;t=5.694,P=0.004)and N-cadherin(t=6.480,P=0.003;t=7.446,P=0.001).Furthermore,Oe-circ_0067582 significantly inhibited the growth of tumor in the SGC-7901 tumor-bearing nude mice(t=3.526,P=0.017).The prediction based on TargetScan and miRnada suggested that hsa_circ_0067582 can competitively bind to hsa-miR-181b-3p,hsa-miR-337-3p,hsa-miR-421,and hsa-miR-548d-3p.The functional enrichment indicated that the target genes of miRNA were involved in multiple cancer-related biological processes including negative regulation of apoptotic process,gene expression,transcriptional misregulation in cancer,transforming growth factor-β,and p53 signaling pathways. Conclusion Oe-circ_0067582 can inhibit the proliferation and attenuate EMT process to reduce the invasion ability of AGS and SGC-7901 cells,which provides a new target for the treatment of GC.
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Animals , Mice , Cell Proliferation , Gene Expression Regulation, Neoplastic , Mice, Nude , RNA, Circular , Stomach Neoplasms/pathologyABSTRACT
@#[Abstract] Objective: To investigate the effect of apatinib (APA) combined with cisplatin (DDP) on the proliferation, invasion and migration capacity of gastric carcinoma (GC) cells and its molecular mechanism. Methods: Cancer and para-cancerous tissue samples resected from 50 GC patients, who were surgically treated in Wuwei People's Hospital from January 2016 to June 2019, were collected for this study; in addition, GC cell lines MGC803 and SGC7901 were also collected. qPCR was used to detect the HMGA2 expression in tissues and mRNA expressions of molecules related to cell proliferation, migration and invasion in GC cell lines. MGC803 and SGC7901 cells were transfected with pcHMGA2 by liposome transfection technology. After treatment with DDP and APA at different concentrations, the cells were divided into NC, pcHMGA2, pcHMGA2+DDP and pcHMGA2+DDP+APA groups. Protein expression of HMGA2 in GC cells was detected by Western blotting, and proliferation, migration and invasion of the cells were detected by MTT and Transwell assay, respectively. Results: The mRNA expression of HMGA2 in GC tissues was higher than that in para-cancerous tissues (P<0.05), and the survival rate of GC patients in the high expression group was significantly reduced (P<0.01). DDP significantly inhibited the proliferation, invasion and migration of MGC803 and SGC7901 cells (all P<0.01); the proliferation, invasion and migration of MGC803 and SGC7901 cells in DDP+APA group significantly decreased (all P<0.01) as compared with DDP group; APA significantly enhanced the inhibitory effect of DDP on HMGA2 expression in GC cells (P<0.01); APA enhanced the anticancer activity of DDP against GC by down-regulating HMGA2 expression. Conclusion: APA promotes the anticancer activity of DDP against GC, and its molecular mechanism is the promotion of the inhibitory effect of DDP on HMGA2 expression.
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Objective To investigate the effect of trichostatin A (TSA) on migration and invasion in human gastric carcinoma SGC-7901 cells and its possible mechanism. Methods SGC-7901 cells were cultured in vitro and treated with TSA (5, 10, 20, 40, 80, 160 nmol/L) for 48 hours, and then the cell viability was detected by cell counting kit 8 (CCK-8) assay. The protocadherin 9 (PCDH9) high-expression SGC-7901 cells were stably established by transfecting with eukaryotic expression vector (pCMV6-PCDH9). Transwell assay was used to determine the abilities of migration and invasion. The mRNA expression level of PCDH9 were measured by RT-PCR. Western blotting was performed to analyze the protein expression of PCDH9, Snail, E-cadherin, matrix metalloproteinase (MMP)-2 and MMP-9. Results TSA remarkably reduced the cell viability of SGC-7901 cells in excess of 80 nmol/L (P<0. 05). However, in a dose-dependent manner, low-level TSA (5-20 nmol/L) suppressed migration and invasion of SGC-7901 cells (P<0. 05), down-regulated the protein levels of Snail, MMP-2 and MMP-9 (P<0. 05), and up-regulated the protein levels of PCDH9 and E-cadherin (P<0. 05). Meanwhile, high expression of PCDH9 also inhibited migration and invasion of SGC-7901 cells (P<0. 05), down-regulated the protein levels of Snail, MMP-2 and MMP-9 (P<0. 05), and up-regulated the protein level of E-cadherin (P<0. 05). Conclusion TSA may inhibit migration and invasion of SGC-7901 cells most likely via up-regulating PCDH9, and then down-regulating the protein levels of Snail, MMP-2 and MMP-9, and up-regulating the protein level of E-cadherin.
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@#Objective: To investigate the effects of ginsenoside Rg3 on the formation of vasculogenic mimicry (VM) in gastric cancer cell line SGC7901 and its molecular mechanism. Methods: MTT assay was used to detect the effect of different concentrations of Rg3 on the proliferation of SGC7901 cells. SGC7901 cells were grouped as follows: BML-284 group, XAV-939 group, Rg3 group, Rg3+ BML-284 group and blank group. Transwell chamber assay was used to detect cell invasion and migration; the formation of VM was observed by tube formation assay; the secretion of MMP-9 and MMP2 was detected by ELISA; the mRNA expressions of GSK-3β and Wnt2B were detected by qPCR; the expression of β-Catenin protein in cells was analyzed by WB; and nuclear entry of β-Catenin was examined by Immunofluorescence. Results: Ginsenoside Rg3 inhibited the proliferation of SGC7901 cells in a time- and concentrationdependent manner; compared with the blank group, 40 mg/L Rg3 significantly inhibited the invasion and migration of SGC7901 cells (both P<0.05) and VM formation (P<0.05); in the meanwhile, the expressions of intracellular GSK-3β, Wnt2B mRNA and β-catenin protein, as well as the nuclear entry of β-catenin were significantly inhibited (all P<0.05). The invasion, migration and VM formation of SGC7901 cells in Rg3+BML-284 group were not significantly different from those in the blank group (all P>0.05). Conclusion: Rg3 can inhibit cell invasion, migration and VM formation in SGC7901 cells by inhibiting the activation of Wnt/β-Catenin pathway.
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@#Objective:To explore the mechanism of EYA1 (eyes absent 1) inhibiting the malignant progression of gastric cancer SGC7901 cells through regulating PTEN/PI3K/AKT signaling pathway. Methods: Twenty-nine pairs of gastric cancer tissues and para-cancerous tissues collected at the General Surgery center, Southwest Hospital Affiliated to Military Medical University during June 2016 and June 2018 were used in this study. Wb and RT-PCR assays were used to test the mRNA and protein expressions of EYA1 in gastric cancer tissues and the paired para-cancerous tissues; Transfection with plasmid or siRNAs were used to up-regulate or down-regulate EYA1 or PTEN expression in gastric cancer SGC-7901 cells; MTT, Flow Cytometry, Wound Healing and Transwell assays were carried out to detect cell proliferation, apoptosis, metastasis and invasion abilities, respectively. Results: EYA1 expression was decreased in gastric cancer tissues as compared with the para-cancerous tissues at both mRNA and protein levels (P<0.01); EYA1 over-expression significantly enhanced the proliferation, metastasis and invasion of SGC-7901 cells (all P<0.05), and inhibited cell apoptosis (P<0.05); moreover, its over-expressionsignificantly increased the expression of PTEN, and inhibited the activation of PI3K/AKT pathway (all P< 0.05 or P<0.01). However, the above effects mediated by EYA1 up-regulation were significantly impaired after the knockout of PTEN (all P<0.05 or P<0.01). Conclusion: EYA1 can inhibit the malignant progression of gastric cancer SGC-7901 cells through promoting the expression of PTEN and activating PI3K/AKT pathway.
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@#[Abstract] Objective: To investigate the effect of Xihuang (XH) extract on the proliferation of gastric cancer SGC-7901 cells and its underlying mechanism. Methods: Gastric cancer cell line SGC-7901 was conventionally cultured. CCK-8 assay and flow cytometry were used to detect the effect of different concentrations of XH extracts (3.2, 6.4, 12.8, and 25.6 mg/ml) on proliferation and apoptosis of SGC-7901 cells after treatment for different time periods (24, 48, and 72 h); The effect of different concentrations of XH extracts on the mRNA expression of apoptosis-related genes (Bax and Bcl-2) was detected by qPCR; Western blotting was used to detect the effect of XH extracts on the expression of apoptosis-associated proteins (caspase 3, caspase 9, Bax and Bcl-2). Results: XH extracts (3.2, 6.4, 12.8, and 25.6 mg/ml) could effectively inhibit proliferation of gastric cancer SGC-7901 cells (P<0.05 or P<0.01) in a concentration-depend manner (P<0.01). XH extract could significantly up-regulate Bax mRNAand down-regulate Bcl-2 mRNAexpression (P<0.05 or P <0.01); Meanwhile, XH extract ouldincrease protein expressions of caspase 3, caspase 9, Bax but reduce Bcl-2 protein expression (P< 0.05 or P<0.01). Conclusion: XH extract can inhibit the proliferation of gastric cancer SGC-7901 cells by triggering apoptosis, which may become a potential method of adjuvant treatment of gastric cancer.
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@# Objective: To investigate the expression of histone methyltransferase G9a in gastric cancer tissues and its correlation to prognosis, and to observe the effect of G9a inhibitor on the proliferation and apoptosis of gastric cancer cells. Methods: The expression level of G9a in gastric cancer tissues and its correlation to prognosis were analyzed by using the Kaplan-Meier Plotter and Oncomine database. Human gastric cancer cell line SGC-7901 and MKN-45 were selected as study subject. The expression level of G9a protein was detected by Western blotting. The morphological change of gastric cancer cells after the treatment of G9a inhibitor BIX01294 was observed. CCK-8 proliferation experiment and plate colony formation assay were used to examine the proliferation ability and clone formation rate of gastric cancer cells. The changes of cell apoptosis were detected by Annexin-V staining. Results: G9a was highly expressed in gastric cancer tissues (P<0.01), and the high expression of G9a was positively correlated with poor prognosis of gastric cancer patients (P<0.01). After the treatment of BIX01294, the morphology of gastric cancer cells was changed, the volume of gastric cancer cells reduced, the intercellular connections disappeared, and even the apoptotic manifestations appeared, such as the shrinking,, becoming round and cast-off etc. BIX01294 could significantly inhibit the proliferation and colony formation but promote the apoptosis of gastric cancer cells (all P<0.05). Conclusion: Histone methyltransferase G9a was highly expressed in gastric cancer tissues, and its high expression level was positively correlated with poor prognosis. The proliferation of gastric cancer cells was obviously inhibited while the apoptosis was significantly promoted after inhibiting G9a expression.
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[Objective] To investigate the effects of platycodin D(PD) on the proliferation and apoptosis of human stomach cancer SGC7901 and the related mechanism.[Methods] SGC7901 was cultured in virto and was treated with 5～20μm·L-1 concentrations of PD.Cell proliferation was examined by MTT assay.Cell apoptosis was detected by Annexin V FITC/PI double staining.The change of mitochondrial trans-membrane potential was measured by JC-1 staining.The potein expression of cleaved caspase-3,cleaved caspase-9,cleaved PARP,bcl-2,bax,p-ERK,ERK,p-JNK,JNK,p-p38 and p38 detected by Western blot.[Results] MTT results showed that PD inhibited the growth of SGC7901 cells in a dose-dependent manner at 24h and 48h.SGC7901 cells treated with PD for 24h showed significantly enhanced apoptosis and weakened mitochondrial membrane potential compared with the control cells.Western blot results showed that PD could up-regulate expression of cleaved PARP,cleaved caspase-3,cleaved caspase-9,bax,p-JNK,p-p38 protein,decreased bcl-2,p-ERK protein,the expression of ERK,JNK,p38 protein did not change significantly.[Conclusion] PD may inhibit the proliferation and induce the apoptosis of SGC7901 cells.These findings indicated that PD inhibited cell proliferation by inhibiting the ERK signaling.PD effect on bax and bcl-2 by activation of JNK and p38 signaling pathway resulted in the decrease of mitochondrial membrane potential and activation of caspase,which induced the apoptosis of cancer cells.
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Background and purpose:EPHA2 has been reported to enhance the proliferation of gastric cancer cells through promoting CyclinD1 expression and cell cycle progression. However, the underlying mechanism that EPHA2 promotes CyclinD1 expression and cell cycle progression is still poorly understood. Akt/mTOR signaling pathway has been reported to enhance the proliferation of gastric cancer cells by promoting CyclinD1 expression and cell cycle progression, and some studies have shown that EPHA2 can activate Akt/mTOR signaling pathway. Based on this, this study investigated whether EPHA2 promoted gastric cancer SGC-7901 cell proliferation through enhancing Akt/mTOR signaling pathway.Methods:Western blot was used to determine the effect of EPHA2 overexpression or knockdown on the phosphorylation of Akt and mTOR in SGC-7901 cells. SGC-7901-NC infected with control lentivi-rus and SGC-7901-EPHA2 cells with EPHA2 overexpression were treated with DMSO, MK2206 (an Akt inhibitor) and RAD001 (a mTOR inhibitor) for different time periods, respectively. Cell proliferation was detected using the CCK8 assay. Cell cycle was detected using lfow cytometry, and the expression of CyclinD1 was determined by Western blot. Results:Overexpression of EPHA2 enhanced Akt/mTOR signaling pathway in SGC-7901 cells, and silencing EPHA2 in SGC-7901 cells inhibited Akt/mTOR signaling pathway. MK2206 and RAD001 antagonized the promoting effect of EPHA2 on the proliferation, S-phase and CyclinD1 expression of SGC-7901 cells, respectively.Conclusion:EPHA2 promotes SGC-7901 cell proliferation through enhancing Akt/mTOR signaling pathway. Akt inhibitor or mTOR inhibi-tor could be an effective treatment strategy for gastric cancer patients overexpressing EPHA2.
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To explore the effects of Celastrus orbiculatus extract (COE) on the expressions of apoptosis-related proteins and growth of human gastric adenocarcinoma SGC-7901 cell xenografts in nude mice. Thirty-five mice with subcutaneous xenografts of a gastric cancer cell line (SGC-7901) were randomly divided into five groups: a negative control group, a positive control group (xeloda), and low-dose, medium-dose, and high-dose COE groups (10, 20, and 40 mg/kg, respectively). There were seven mice in each group. Tumor volume, tumor weight, and body weight were measured to draw up tumor growth curves and the tumor weight inhibition rates were calculated. The apoptosis rates were measured by TUNEL staining method and the expressions of p53, Bcl-2, and Bax proteins were detected by immunohistochemical staining and Western blotting assay. The COE could inhibit the growth of SGC-7901 xenografts in a dose-dependent manner. The tumor inhibitory rates were 33.3%, 46.8%, and 57.7% when treated with 10, 20, and 40 mg/kg COE, respectively. TUNEL assay showed that COE presented with apparently more apoptosis than the negative control group. The results of immunohistochemical staining showed the expressions of p53 and Bax proteins had a trend of up-regulation, while the expression of Bcl-2 protein had a trend of down-regulation in nude mice after treatment with COE. Compared with the negative control group, the expressions of p53 and Bax were significantly up-regulated, while the expression of Bcl-2 was down-regulated in the high-dose COE group. Western blotting analysis showed the similar results to immunohistochemical staining. COE could significantly inhibit the growth of SGC-7901 cell xenografts in nude mice, which might be related with the up-regulation of the expressions of p53 and Bax and down-regulation of the expression of Bcl-2.
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Objective_To study the effect of Y-27632 on invasion and motility of SGC-7901 gastric carcinoma cells, and to find whether Y-27632 excerts the effect by attenuating SRF expression.Methods_SGC-7901 gastric carcinoma cells were divided into 3 groups:1)blank control group;2)Y-27632 group;3)siRNA-SRF-1107 group. Transfected siRNA-SRF or incubated by Y-27632 48 h.The effect of Y-27632 on proliferation suppressions of SGC-7901 gastric carcinoma cells was detected by CCK-8 assay.Cell invasion was examined by Transwell and wound healing test.The expression of SRF, ROCK1, E-cadherin, β-catenin, F-actin, MRTF-A and Cyclin D1 were detected by Western blot.Results_Y-27632 inhibited invasion (P<0.05)but had no effect on proliferation of SGC-7901 gastric carcinoma cells.Y-27632 reduced ROCK1, MRTF-A, F-actin, SRF protein expressions by 37.0%, 44.3%, 62.7%and 62.7%respectively, and E-cadherin protein expression was up-regulated by 2.64 folds(P<0.05).Conclusions_The inhibition of ROCK and up-regulation of E-cadherin by Y-27632 can inhibit the invasion and migration of SGC-7901 gastric carcinoma cells that is explained at least, in part, by attenuating SRF expression.
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OBJECTIVE:To study the effects of flow components C6 and C7 in n-butyl alcohol extract from the leaves of Ces-trum Nocturnum(CN)on the proliferation and apoptosis of human gastric cancer cell SGC7901. METHODS:C6 and C7 were ob-tained by using different ratio of chloroform and methanol(1:9,1:7)to the gradient elution of CN leaves. After cultured with 0 (blank control),5,10,20,40,80 μg/ml C6 and C7 for 72 h,inhibitory effect of C6 and C7 on the proliferation of SGC7901 was determined by MTT assay. Inhibitory rate and IC50 were calculated. After SGC7901 were cultured with 10 μg/ml C6 and C7 for 72 h,colony formation assay was utilized to detect the effects of C6 and C7 on the cell colony formation,and the rate of colony for-mation was calculated. In addition,Wright/Giemsa and Hoechst33258/PI staining assay were used to observe the change of cytomor-phology. RESULTS:MTT showed that C6 and C7 had inhibitory effect on the proliferation of SGC7901 to different extent;inhibi-tory rates were 22.1%-80.0% and 19.6%-79.7%,and IC50 were 16.4,18.05 μg/ml,respectively. Compared with blank control group,colony formation rate of C6 and C7 group decreased,with statistical significance(P<0.05). The number of apoptotic cells was more in treatment group than in other groups. CONCLUSIONS:Flow components C6 and C7 in n-butyl alcohol extract from the leaves of CN can inhibit the proliferation of SGC7901 cells and induce the apoptosis of them.
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Objective To encode the protein cystatin M with CST6 gene and construct a CST6-overexpression vector,and transfect it into the gastric cancer cells SGC-7901 in order to observe the effect of cystatin M on the proliferation and migration abilities of SGC-7901 cells.Methods There were three groups in the experiment:pcDNA3.1(+)-CST6 group,pcDNA3.1 (+)group and non-transfected group.RT-PCR and Western blot were used to identify the RNA expression of CST6 in SGC-7901/CST6 cells.The proliferation and migration abilities of the transfected cells were detected by MTT and cell wound healing assay,respectively.Results SGC-7901/CST6 cells stably expressed CST6 gene RNA and cystatin M protein.The proliferation and migration of pcDNA3 .1 (+)-CST6 group cells were reduced compared with those of cells in the other two groups (P<0.05).Conclusion Cystatin M can inhibit the proliferation and migration of SGC-7901 cells.
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Objective To investigate the effect of metformin on human gastric cancer line SGC-7901 in vitro, trying to explore the mechanism involved. Methods Human gastric cancer SGC-7901 cell was cultured in vitro, MTT was used to study the effects of metformin on cell growth with different concentration or different time. Western blot was used to investigate the influence of metformin on the expression of Cyclin Dl in cell line . Results The result of MTT showed human gastric cancer SGC-7901 cell was cultured in vitro and was exposed to metformin in different concentration (50 mmol/L, 100 mmol/L) for 24 h,48 h,72 h. The inhibitory rates of 50 mmol/L metformin on the effects of metformin on cell growth was 32.93% ,48.64% and 61.40% and the inhibitory rates of 100 mmol/L metformin on the effects of metformin on cell growth was 35.34% , 75.44% and 88.30%. The proliferation of SGC-7901 cell was inhibited by different concentration (50 mmol/L, 100 mmol/L) metformin and,the inhibitory rates were significantly decreasing compared with the control group(P < 0.05).The inhibitory rate treated with 100 mmol/L metformin was significantly decreasing compared with 50 mmol/L metformin group (P < 0.05). The inhibitory rate treated with metformin at different time(24 h,48 h, 72 h) was significantly different(P <0.05). Metformin could inhibit the proliferation of SGC-7901 cells, with dose and time-related effects. Cyclin Dl expressed in high level in SGC-7901 and metformin significantly decreased the expression of Cyclin Dl, with dose and time-related effects. Conclusion metformin could inhibit the proliferation and lower the expression of Cyclin Dl in human gastric cancer line SGC-7901 in vitro.
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Aim To explore the effects of the Melittin on growth and cell cycle of SGC-7901 cells.Methods Growth inhibition effect of Melittin was evaluated using SRB in SGC-7901 cells in vitro;Melittin induced cell cycle arrest was investigated using flow cytometry assay;reverse transcription PCR(RT-PCR)was used to detect the associated protein mRNA of cell cycle.Results Proliferation activity of SGC-7901 cells was inhibited after treatment with Melittin(1,2,4,8,16,32×10~(-3) μg·L~(-1))(P<0.05 or P<0.01)for 24 h;Flowcytometry analysis revealed that SGC-7901 cells accumulated in the G_2/M phase after treatment with Melittin(4,8×10~(-3) μg·L~(-1))for 24 h;the expression of CylinB1,CDK1 and Cdc25c mRNA were decreased.Conclutions Proliferation activity of SGC-7901 cells was inhibited by Melittin,which may be related to the inhibitory effect of Melittin on associated protein transcription in the G_2/M stage of SGC-7901 cells.
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Aim To investigate the effects of Aplysin on the inhibition of gastric cancer cell in vitro .Methods MTT assay was used to examine the inhibition of gastric cancer cell 1ine SGC-7901 by Aplysin in different concentrations and at different times.The morphologic changes and the apoptosis of SGC-7901 was observed by inverted microscope and Hematoxylin-Eosin(HE)staining.Reverse transcriptase polymerase chain reaction(RT-PCR)assay was used to detect the changes of COX-2 mRNA expressions.Results Aplysin could decrease the proliferation significantly in a dose-dependent manner in SGC-7901 cells.When treating SGC-7901 with Aplysin in concentration of 120, 240 mg·L~(-1) for 24 h, the growth of the cell was obviously inhibited observing by inverted microscope.Aiso, when treating with the same concentration for 18 h, its chromatin became crimpled and breakdown, as well as cell shrinkage and apoptotic bodies formation when using HE staining.The apoptotic rates(%)of SGC-7901 was(15.0±2.12)%, (18.4±2.3)%, respectively, which was significantly higher than(1.4±0.55)% that in control group(P <0.01).60、120、240 mg·L~(-1) Aplysin could not effectively inhibited the mRNA expressions of COX-2(P ＞0.05).Conclusions Aplysin can inhibit the proliferation and induces apoptosis of SGC-7901 cells.
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Objective To explore the effect of Wuji Solution (He Ji Ju Fang) on excreting IL-8 of SGC-7901 cells infected with Helicobacter pylori (H?pylori) in vitro. Methods H?pylori was inoculated to SGC-7901 cells. ELISA was applied to examine the production of interleukin-8 (IL-8) of cells infected with H?pylori. Results The production of IL-8 of infected cells was lower than that of control group (P
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Objetive: To investigate whether apoptosis of SGC7901 cells can be induced by the expression of the recombinant gene of anti-HER2 ScFv/tBid. Methods: The recombinant anti-HER2 ScFv/tBid gene was cloned into vector pCMV and the recombinant plasmid was transfected into SGC7901 cells. The gene expression was detected by RT-PCR and immunofluorescent staining. Cell counting was carried out to show the effect of the gene transfection on cell growth. At the same time, significant apoptotic peak was detected by flow cytometry in recombinant anti-HER2 ScFv/tBid gene transfected cells. Results: The fusion protein of anti-HER2 ScFv/tBid was observed in the cytoplasm of transfected SGC7901 cells. The transfected cells displayed typical cell growth inhibition and apoptosis. Conclusion: Fusion protein of anti-HER2 ScFv/tBid can induce apoptosis of SGC7901.
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Objective To study the effects and mechanism of Octreotide to inhibit the proliferation of human gastric cancer cells in vitro . Methods Human gastric cancer cell line SGC 7901 was treated with Octreotide. Human fibroblast cell line HF and 5 FU were used as control. MTT assay and fluorescent microscopy as well as flow cytometry were performed in this study. Results Octreotide inhibited the growth of SGC 7901 in vitro within certain concentrations. The suppression was quantity dependent but did not occur when up to a certain concentration. There was no difference between Octreotide and 5 FU in their inhibition on SGC 7901. Octreotide had no effects on normal human fibroblast cell line HF. When SGC 7901 was treated with Octreotide, the typical apoptotic bodies were identified by flow cytometry and fluorescent microscopy. Conclusion Octreotide can inhibit the proliferation of human gastric cancer cell line SGC 7901 in vitro . The induction of apoptosis by Octreotide might be the primary mechanism.
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Objective:To construct pEGFP-C1-Smad4 expression vector and to observe the influence of Smad4 over-expression on the proliferation of human gastric cancer SGC7901 cells and its relationship with nuclear factor kappa B (NF-?B). Methods:Recombinant expression vector pEGFP-C1-Smad4 was constructed and was used to transfect human gastric cancer SGC7901 cells. EGFP expression in transfected cells was detected by fluoroscopy. Smad4 and NF-?B expression in transfectant was examined by Western blotting. Effect of Smad4 over-expression on activation of NF-?B and proliferation of transfected SGC7901 cells were examined by electrophoretic mobility shift assay (EMSA) and MTT assay,respectively. Results:Expression of EGFP in transfected SGC7901 cells was observed under fluorescence microscope. Smad4 was over-expressed in transfected SGC7901 cells,accompanied by down-regulation of NF-?B p65 expression in the tranfectants. EMSA and MTT demonstrated that Smad4 over-expression significantly inhibited the activation of NF-?B and the proliferation of SGC7901 cells (P