Invasion Of BGC-823 Cells Research Articles

Effect of lentivirus-mediated peroxiredoxins 6 gene silencing on the phenotype of human gastric cancer BGC-823 cells.

Peroxiredoxins (PRDX6) regulates the occurrence and progression of cancer. The aim of this study is to investigate the effect of PRDX6 knockdown on the biological behavior of human gastric cancer cell line BGC-823 cells. Research article. The differential expression of PRDX6 in gastric cancer and normal gastric tissues was tested by immunohistochemistry. Ribonucleic acid plasmid of PRDX6 gene was packaged using a lentivirus, and BGC-823 cells were transfected with the lentivirus to obtain a BGC-823 cell line in which the expression of PRDX6 was stably silenced. The proliferation activity of BGC-823 cells was detected using the cell counting kit-8 method. The effect of PRDX6 on the migration and invasion of BGC-823 cells was evaluated using the scratch test and Transwell assay, and the expression of related proteins was detected by western blot. The expression of PRDX6 in gastric cancer was significantly increased (P < 0.05). Compared with those in the untransfected and negative control groups. The proliferation, migration, and invasion of gastric cancer BGC-823 cells were significantly inhibited, and the apoptotic rates were significantly increased in the lentivirus-transfected (short hairpin-PRDX6) group. Western blot analysis showed that the expression of Bax protein increased, whereas that of proliferating cell nuclear antigen, Bcl-2, PI3K, phospho (p-Akt), and phosphorylated-mammalian target of rapamycin (mTOR) decreased significantly compared with that in WT and vector groups (P < 0.05). The knockdown of PRDX6 gene expression in BGC-823 cells can inhibit the proliferation, migration, and invasion of gastric cancer cells and promote apoptosis, thereby affecting gastric cancer cells.

Long noncoding RNA LINC00858 promotes the proliferation, migration and invasion of gastric cancer cells via the miR-363-3p/FOXP4 axis.

Long non-coding RNA (lncRNA) LINC00858 has been found to exert oncogenic activity in several types of cancers, except gastric cancer (GC). In the present study, we aimed to explore the potential role of LINC00858 in GC and the underlying molecular mechanism. The expression patterns of LINC00858 were determined using qRT-PCR in GC samples and cell lines. Cell proliferation was examined utilizing CCK-8 assay. Cell migration and invasion were evaluated using transwell assays. We used the bioinformatics software StarBase and TargetScan to predict lncRNA-miRNA and miRNA-mRNA interactions. Our findings revealed that LINC00858 expression was markedly upregulated in GC tissues and cell lines. Loss-of-function experiments demonstrated that LINC00858 silencing inhibited the proliferation, migration and invasion of GC cells. Bioinformatics analysis showed that there were several complementary binding sites between LINC00858 and microRNA (miR)-363-3p, and further Luciferase reporter assay confirmed the interaction between LINC00858 and miR-363-3p. In addition, forkhead box P4 protein (FOXP4) was found to be a target gene of miR-363-3p in GC cells. FOXP4 overexpression reversed the inhibitory effects of miR-363-3p mimics on cell proliferation, migration and invasion of BGC-823 cells. Collectively, LINC00858 acted as an oncogene in GC via regulating miR-363-3p/FOXP4 axis, which indicated that LINC00858 might be a novel therapeutic target for the treatment of GC.

Impact and mechanism of Loganin on epithelial mesenchymal transformation of gastric cancer cells

Objective To explore impact and molecular mechanism of Loganin on epithelial mesenchymal transformation of gastric cancer cells. Methods Human gastric cancer cell lines AGS, BGC823 and SGC7901 were cultured routinely. The effect of Loganin on cells activity was tested by utilizing methyl thiazol tetrazolium (MTT) assay. Also Wound assay and Transwell assay were employed to detect the effect of Loganin on migration and invasion in BGC823 cells. Furthermore, real-time quantitative reverse transcriptase-polymerase chain reaction (RT-qPCR) and Western blotting were used to examine the variations of associated genes and phosphatidylinositol 3 kinase (PI3K)-protein kinase B (Akt) signal pathway in BGC823 cells prior and post Loganin interventions. Results Results of MTT assay showed that the activity of BGC823 was lowest among AGS (0.748±0.051), BGC823 (0.581±0.042) and SGC7901 (0.412±0.037) (F=44.101, P<0.01); the expression level of PCNA mRNA and protein declined gradually with the increase dose of Loganin (F=36.298, 47.942, P<0.01). Compared with the control group, the ability of migration and invasion in BGC 823 cells decreased, and this changes were particularly distinct in high dose Loganin group (200 mg/L), which were more significant than in low dose group (50 mg/L) (migration: F=87.750, P<0.01; invasion: F=85.749, P<0.01). Results of qPCR and Western blotting showed that expressions of migration, invasion associated genes in BGC823 cells changes significantly compared with the control group, especially in high dose Loganin group (P<0.01). Results of qPCR and Western blotting illustrated that EMT related gene in BGC823 cells changes significantly compared with the control group, especially in high dose Loganin group (P<0.01). The activity of PI3K-Akt signal pathway declined significantly post Loganin intervention, and expression of p-PI3K, p-Akt decreased significantly, especially in high dose Loganin group (F=38.590, 63.563; P<0.01). Conclusion Loganin may inhibit EMT in gastric cancer cells via regulating PI3K-Akt signal pathway. Key words: Gastric cancer; Loganin; Invasion; Epithelial mesenchymal transformation; Phosphatidylinositol 3 kinase-protein kinase B signal pathways

DZNep inhibits Hif-1α and Wnt signalling molecules to attenuate the proliferation and invasion of BGC-823 gastric cancer cells.

3-deazaneplanocin A (DZNep) is a histone methyltransferase inhibitor, which may cause the reactivation of silenced tumor suppressor genes in tumors to inhibit the development, metastasis and dissemination of tumor cells. However, the effects and mechanisms of its application in gastric cancer remain unclear. The present study revealed an inhibitory function of DZNep in BGC-823 cells. The cell colony, Cell Counting Kit-8 (CCK8), wound healing, Transwell and flow cytometry assays were performed, and the results demonstrated that DZNep could inhibit the proliferation, apoptosis and invasion of BGC-823 cells, and promote their apoptosis. The effects of intervention in BDC-823 cells with DZNep on the RNA and protein expression levels of hypoxia-inducible factor (Hif-1α) and Wnt/β-catenin signalling molecules were further examined using reverse transcription-quantitative PCR and western blot analysis. The results demonstrated that different concentrations of DZNep could inhibit the expression of enhancer of zeste homolog 2 (EZH2) protein, decrease the RNA and protein expression levels of Hif-1α, total β-catenin and phosphorylated-β-catenin and increase the expression levels of non-phosphorylated-β-catenin to different degrees. The results of the present study suggests that DZNep inhibits BGC-823 gastric cancer cells via the inhibition of EZH2, Hif-1α and Wnt/β-catenin signalling molecules. These results provide theoretical basis for the application of DZNep in clinical trials.

Elevated limb-bud and heart development (LBH) expression indicates poor prognosis and promotes gastric cancer cell proliferation and invasion via upregulating Integrin/FAK/Akt pathway

The limb-bud and heart development (LBH) gene is a highly conserved, tissue-specific transcription cofactor in vertebrates that regulates multiple key genes in embryonic development. The role of LBH in various cancer types is still controversial, and its specific role and molecular mechanism in the oncogenesis of gastric cancer (GC) remains largely unexplored. In the present study, the prognostic significance and clinicopathological characteristics of LBH in GC was determined. The LBH mRNA expression was first investigated in four independent public datasets (TCGA-STAD, GSE15459, GSE29272, and GSE62254) and then validated with our samples at the protein level. LBH was overexpressed at both the mRNA and protein levels in cancer compared with normal tissues. High LBH expression was correlated with advanced T, N, and M stages. Kaplan–Meier analysis and log-rank test indicated that higher LBH expression was statistically correlated with shorter overall survival (OS) in the public datasets and our study samples. Univariate and multivariate Cox regression analysis showed that LBH was an independent prognostic biomarker for survival in TCGA-STAD, GSE15459, GSE62254 cohorts, and our GC patients. In vitro experiments showed that knockdown of LBH can significantly inhibit the proliferation and invasion of HGC-27 cells, while overexpression of LBH can significantly enhance the proliferation and invasion of BGC-823 cells. Gene Set Enrichment Analysis (GSEA), Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomics (KEGG) indicated that high LBH expression is associated with the PI3K-Akt pathway, focal adhesion, and extracellular matrix (ECM)-receptor interaction. Western blot analysis showed that knockdown of LBH significantly inhibited the expression of integrin α5, integrin β1, p-FAK, and p-Akt. Therefore, results from the present study indicate that LBH is a potential independent prognostic biomarker and promotes proliferation and invasion of GC cells by activating the integrin/FAK/Akt pathway.

Long noncoding RNA STCAT16 suppresses cell growth and its expression predicts prognosis in patients with gastric cancer.

Gastric cancer (GC) is a leading cause of cancer-associated mortality worldwide. Previous studies demonstrated that long noncoding RNAs (lncRNAs) may be dysregulated in GC and may serve important roles in cancer progression. The present study aimed to investigate the role of the novel lncRNA stomach cancer-associated transcript 16 (STCAT16; Assembly Gene ID G038291) in the development and progression of GC. The present data suggested that the expression level of STCAT16 was decreased in GC tissues. The expression level of STCAT16 was identified to be associated with lymph node and tumour node metastasis stages. Furthermore, the expression level of STCAT16 was identified to be significantly associated with poor survival and prognosis. Knockdown of STCAT16 promoted proliferation, colony formation, migration and invasion of BGC-823 cells. In contrast, these features were suppressed in AGS cells following overexpression of STCAT16. In vivo, tumour growth was significantly decreased following STCAT16 overexpression. Collectively, the present data suggested that the lncRNA STCAT16 may act as a tumour suppressor and may inhibit GC tumour cell growth and migration. Additionally, the decreased expression level of STCAT16 was identified to be associated with poor prognosis in patients with GC.

Anti-neuropilin-1 monoclonal antibody suppresses the migration and invasion of human gastric cancer cells via Akt dephosphorylation.

Neuropilin-1 (NRP-1) is involved in a range of physiological and pathological processes, including neuronal cell guidance, cardiovascular development, immunity, angiogenesis and the pathogenesis of cancer. Targeting of NRP-1 is considered to be a potential cancer therapy and a number of approaches have been investigated, including the use of small interfering RNA, peptides, soluble NRP antagonists and monoclonal antibodies. The present study used a novel anti-neuropilin-1 monoclonal antibody (anti-NRP-1 mAb) to investigate its potential anti-tumor effects on human gastric cancer cells in vitro and in vivo, as well as its underlying mechanisms of action. Using an MTT assay, it was observed that anti-NRP-1 mAb (<150 µg/ml) had no effects on the viability of gastric cancer cell line BGC-823, while a Boyden chamber assay indicated that treatment with anti-NRP-1 mAb suppressed the migration and invasion of BGC-823 cells. Western blot analysis also demonstrated that phosphorylation of Akt was reduced in BGC-823 cells treated with anti-NRP-1 mAb. Furthermore, anti-NRP-1 mAb suppressed the growth of gastric cancer xenograft tumors and downregulated the expression of vascular endothelial growth factor proteins within tumors in nude mice. These data indicate the potential effects of anti-NRP-1 mAb on malignant tumors and suggest that inhibition of NRP-1 function with anti-NRP-1 mAb may be a novel therapeutic approach in the treatment of cancer.

Interleukin-23 promotes the migration and invasion of gastric cancer cells by inducing epithelial-to-mesenchymal transition via the STAT3 pathway

Chronic inflammation is associated with all stages of cancer development. Moreover, a proinflammatory microenvironment resulted from chronic inflammation is considered to be an essential component of cancer. Interleukin-23 (IL-23) is a general proinflammatory factor; and is involved in tumor-associated inflammation in gastric cancer (GC). However, the direct effect of IL-23 on GC cells has been rarely reported. The aim of the study was to clarify the direct role of IL-23 in regulating GC progression, and to identify the underlying mechanism. In this study, Positive expression of IL-23R was observed in GC tissues and cell lines by using immunohistochemistry or immunofluorescence. In western blots, the expression of IL-23R was higher in GC tissues compared with adjacent normal tissues. Furthermore, IL-23R positive GC tissues were closely related with larger tumor size and worse T stage and clinical stage. By performing in vitro experiments, we found that IL-23 binding to its receptor promoted the migration and invasion of BGC-823 cells in vitro. Moreover, IL-23 induced the activation of STAT3 and epithelial-to-mesenchymal transition (EMT) in BGC-823 cells. Knocking down STAT3 in BGC-823 cells attenuated the effect of IL-23 on EMT and cell migration and invasion. Taken together, our study has firstly demonstrated the positive expression of IL-23R in human GC tissues and cell lines. IL-23 binding to its receptor promotes the migration and invasion of GC cells by inducing EMT through the STAT3 signaling pathway. This work provides a new mechanism for the oncogenic role of IL-23 on GC progression.

Long non-coding RNA NEAT1 regulates the proliferation, migration and invasion of gastric cancer cells via targeting miR-335-5p/ROCK1 axis.

This study aimed to elucidate the roles of long non-coding RNA Nuclear Paraspeckle Assembly Transcript 1 (NEAT1) in gastric cancer. The expression of NEAT1 in gastric cancer tissues and cells was determined. NEAT1 was then overexpressed and suppressed in BGC-823 cells in vitro to further explore the effects of NEAT1 on cell proliferation, migration, and invasion. In addition, the regulatory relationship among NEAT1, miR-335-5p and Rho Associated Coiled-Coil Containing Protein Kinase 1 (ROCK1) was investigated. LncRNA NEAT1 was upregulated in gastric cancer tissues and cells. Upregulated NEAT1 significantly promoted the proliferation, migration and invasion of BGC-823 cells, while suppression of NEAT1 exhibited contrary results. In addition, lncRNA NEAT1 inhibited the expression of miR-335-5p, and miR-335-5p targeted ROCK1 in BGC-823 cells. miR-335-5p overexpression significantly inhibited cell proliferation, migration and invasion, which was counteracted by ROCK1 overexpression concurrently. Our findings indicate that upregulation of NEAT1 may promote proliferation, migration and invasion of gastric cancer cells via targeting miR-335-5p/ROCK1 axis. NEAT1-miR-335-5p-ROCK1 axis may be a potential therapeutic strategy for gastric cancer therapy.

Effect of lncRNA BNC2-AS1 on the Proliferation, Migration and Invasion of Gastric Cancer Cells.

Background: Gastric cancer is one of the most common cancers and is the second leading cause of cancer mortality worldwide. The present study aimed to investigate the potential biological effect of long non-coding RNA (lncRNA) BNC2-AS1 on the proliferation, migration, and invasion of cervical cancer cells. Methods: BNC2-AS1 small interfering RNA (siRNA) was transfected into SGC7901 and BGC823 gastric cancer cell lines, with negative siRNA serving as a control. A reverse transcription-quantitative polymerase chain reaction assay was performed to confirm the knockdown of BNC2-AS1. Cell Counting Kit (CCK)-8 and colony-forming unit (CFU) assays were performed to evaluate the effect of BNC2-AS1-knockdown on SGC7901 and BGC823 cell proliferation. A wound healing assay was performed to evaluate the effect of BNC2-AS1-knockdown on SGC7901 and BGC823 cell proliferation and migration. A tumor invasion assay was used to evaluate the effect of BNC2-AS1-knockdown on SGC7901 and BGC823 cell invasion. The expression level of BNC2-AS1 was efficiently knocked down by siRNA 48 hours post-transfection. Results: The results of CCK8 and CFU assays showed that BNC2-AS1-knockdown significantly decreased gastric cancer cell proliferation. Wound healing assay results indicated that BNC2-AS1-knockdown markedly suppressed gastric cancer cell proliferation and migration. Tumor invasion assay results demonstrated that BNC2-AS1-knockdown significantly suppressed gastric cancer cell invasion. Conclusions: BNC2-AS1 levels in gastric cancer SGC7901 and BGC823 cell lines can be efficiently knocked down using the siRNA strategy, and the BNC2-AS1 knockdown can significantly suppress the tumor characteristics of gastric cancer cells, including the ability of proliferation, migration, and invasion.

SLC3A2, antigen of mAb 3G9, promotes migration and invasion by upregulating of mucins in gastric cancer.

Solute carrier family 3 member 2 (SLC3A2) has been reported to be highly expressed in a variety of carcinomas. However, the function of SLC3A2 in gastric carcinoma (GC) has not been well explored. Monoclonal antibody (mAb) 3G9, generated from immunogen of various human GC cell lines, has been shown to bind to GC tissues specifically. In this study, we identified the target antigen of mAb 3G9 as SLC3A2, and detected the expression profile of SLC3A2 in a panel of gastric cancer cell lines and GC tumor tissues. We found that the increased expression of SLC3A2 was associated with serosal invasion in GC patients. Knockout of SLC3A2 suppressed the migration and invasion of BGC-823 cells in vitro and in vivo, whereas overexpression of SLC3A2 in NCI-N87 cells promoted the migration and invasion in vitro and in vivo. Mechanistic investigations suggested that MUC1, MUC16 and MUC5B were the downstream genes of SLC3A2 in GC cells. Taken together, our data suggested that SLC3A2 promoted the aggressive phenotype of GC by upregulating several mucin genes expression and may serve as a potential biomarker for diagnosis and target therapy.

The involvement of survivin in insulin-like growth factor 1-induced epithelial-mesenchymal transition in gastric cancer.

It has been identified that insulin-like growth factor 1 (IGF-1) activated various pathways of the epithelial-mesenchymal transition (EMT) in a couple of tumors. At the same time, survivin is implicated in EMT of gastric cancer (GC). To date, the impact of survivin on IGF-1-mediated EMT of GC has not been featured. In this work, we used the immunohistochemistry and molecular and cellular experiments to investigate the existence and significance of IGF-1 and survivin. Our findings revealed that survivin protein can be observed in majority of samples in all GC samples. Importantly, survivin expression has an obvious association with GC stage, and metastasis. In vitro, GC cell line BGC823 was treated with different concentrations of IGF-1, resulting in the activation of p-ERK, p-AKT, survivin, and the expression of EMT biomarkers, including N-cadherin, MMP2, and Snail. However, the silencing of survivin eradicated the expression IGF-1-induced EMT biomarkers and affected the migration and invasion of BGC823 cells. In conclusion, IGF-1 signaling activated survivin expression and controlled the expression of EMT biomarkers in the development of GC. This study lays a new stage for the molecular therapy of GC patients in the clinical treatment.

Significance of FBX8 in progression of gastric cancer

F-box only protein 8 (FBX8), a novel component of F-box proteins, has recently been observed in several malignancies. However, its clinical implication in the progression of gastric cancer still remains unclear. The aim of this study was to explore the role of FBX8 in gastric cancer (GC) and analyze its correlation with tumor progression and prognosis. The expression of FBX8 in GC cell lines and matched pairs of fresh gastric cancer tissues were detected by real-time RT-PCR and Western blotting. Immunohistochemistry was used to analyze clinicopathological patterns of FBX8 in 136 cases of clinical paraffin-embedded GC tissues. A series of functional assays were conducted to evaluate the effect of FBX8 on proliferation and invasion in vitro and metastasis in vivo. FBX8 was markedly down-regulated in GC tissues compared to adjacent normal tissues. Patients with low FBX8 had shorter overall survival time and poor prognosis. Knocking down FBX8 obviously promoted proliferation and invasion in BGC823 cells, while over-expression of FBX8 in SGC7901 and AGS cells had the opposite effects. Moreover, FBX8 was sufficient to suppress metastasis in nude mice. Down-regulation of FBX8 significantly correlates with invasion, metastasis and poor survival time in GC patients. FBX8 may serve as a promising therapeutic target for inhibition of GC metastasis.

Impact on growth and invasion of gastric cancer cell lines by silencing NEDD9.

BackgroundGastric adenocarcinoma is a predominant disease with latent attribute, high malignancy, and poor prognosis in People’s Republic of China. Gastric cancer is the most common malignant tumor of the digestive tract. It has been suggested that abnormal expression of NEDD9 was associated with stage progression and metabolism of carcinomas. Some authors demonstrated that both messenger RNA (mRNA) and protein of NEDD9 were highly expressed in gastric cancer, and paired paracancerous atypical hyperplasia tissues were correlated with lymph node metastasis, tumor depth, and tumor-lymph node-metastasis (TNM) staging. In this study, we found that NEDD9 small interfering RNA (siRNA) can induce apoptosis and suppress proliferation, migration, and invasion of BGC823 cell lines. These findings suggested that NEDD9 siRNA might serve as a tumor suppressor by targeting NEDD9 in gastric cancer cell. It has been suggested that abnormal expression of NEDD9 was associated with carcinogenesis, and in the first part of the study, we found that NEDD9 was highly expressed in gastric cancer tissues; and it too was correlated with lymph node metastasis, tumor depth, and TNM staging. In this project, experiments were carried out to silence NEDD9 in BGC823 cell lines using NEDD9 siRNA, and the biological activity of BGC823 cells was observed after RNA interference.MethodsThe target analysis of NEDD9 siRNA was forecast using online tools. In order to determine a more efficient NEDD9 siRNA, three pairs of NEDD9 siRNA primer were designed, synthesized, and then transfected into BGC823 cells. NEDD9-2 siRNA was finally adopted by detecting the quantitative real-time polymerase chain reaction (qRT-PCR). Cells were collected for detecting mRNA by qRT-PCR or protein by western blot analysis. Cell apoptosis was detected using flow cytometry, and the transwell invasion system was used for cell migration and invasion assays. The effect of NEDD9 siRNA in silencing the target gene in BGC823 cells was then assessed. Also, the impact of NEDD9-2 siRNA on cell proliferation, apoptosis, migration, and invasion were detected in BGC823 cell lines.ResultsThe relative quantity of expression of mRNA and protein showed a decrease in all cells transfected with siNEDD9-2 at different concentrations. The cell proliferation inhibition assay showed that the inhibition rate was significantly increased in all transfected cells compared with control groups. Cell apoptosis assay showed that the number of living cells were significantly reduced compared with control groups, and cell migration and invasion assay showed that siNEDD9 could inhibit BGC823 cell migration and invasion in vitro.ConclusionNEDD9 siRNA could inhibit expression of NEDD9 and induce apoptosis, suppress proliferation, migration, and invasion of BGC823 cells, acting as a tumor suppressor in carcinogenesis of gastric cancer. These findings suggested that NEDD9 siRNA plays an important role in the proliferation, apoptosis, and invasion of BGC823 cells.

Impact of Annexin A3 expression in gastric cancer cells.

Annexin A3 participates in various biological processes, including tumorigenesis, drug resistance, and metastasis. The aim of this study was to investigate the expression of Annexin A3 in gastric cancer and its relationship with cell differentiation, migration, and invasion of gastric cancer cells. Annexin A3 expression in gastric cancer tissues was detected by quantitative real-time PCR and Western blotting. The proliferation of gastric cancer cells was measured by the MTT assay. Cell migration and invasion were determined via wound healing and transwell assays, respectively. Knock down of endogenous Annexin A3 in gastric cancer BGC823 cells was performed using siRNA technology. The expression of Annexin A3 was significantly upregulated in gastric cancer tissues, and negatively correlated with the differentiation degree. Silencing of endogenous Annexin A3 suppressed the proliferation, migration, and invasion of BGC823 cells. Additionally, the expression of p21, p27, TIMP-1, and TIMP-2 was upregulated, and the expression of PCNA, cyclin D1, MMP-1, and MMP-2 decreased in cells treated with Annexin A3-siRNA. Annexin A3 was upregulated in gastric cancer cells. Deletion of endogenous Annexin A3 significantly inhibited gastric cancer cell proliferation, migration, and invasion.

Downregulation of the GnT-V gene inhibits metastasis and invasion of BGC823 gastric cancer cells

Metastatic and invasive potential is a barrier to the successful treatment of gastric cancer. N-acetylgluco-saminyltransferase V (GnT-V), a key enzyme catalyzing the formation of 1,6 N-acetylglucosamine (GlcNAc), has been demonstrated to display a distinct function in different types of tumors. The aim of this study was to investigate the role of GnT-V in the invasive potential of BGC823 human gastric cancer cells invitro and the possible underlying mechanism. GnT-V was downregulated in BGC823 cells by oligo-siRNA transfection. Cell proliferation and invasiveness were assessed by CCK-8 assay, Tunel assay, scratch-wound assay as well as transwell assay. The products of GnT-V, β1-6 branching of asparagine-linked oligosaccharides, were determined by L-PHA lectin blot analysis. The expression of EGFRs, E-cadherin/vimentin and MMP-2/MMP-9 was analyzed both at the mRNA and protein levels. The results showed that downregulation of GnT-V decreased proliferation and the metastatic/invasive potential of BGC823 cells. The expression of EGFRs, E-cadherin/vimentin and MMP-9, molecules related to cancer metastasis and invasion in various tumors, were influenced correspondingly. These findings suggest that downregulation of GnT-V inhibited cell metastasis and invasion of BGC823 cells via EGFR signaling-initiated EMT phenotype and MMP-9 expression. These results provide a novel mechanism to explain the role of GnT-V in cell metastasis and invasion.

Effects of down-regulation of tmnor-associated calcium signal transducer-2 gene expression by RNA interference on adhesion, migration and invasion of gastric cancer cells

Objective To study the effects of tumor-associated calcium signal transducer-2 (TROP-2) gene small interfering RNA (siRNA) on adhesion, migration, and invasion of human gastric cancer cells.Methods Real time polymerase chain reaction (PCR) was used to detect the TROP-2 mRNA expression of human gastric cancer cell lines MGC-803, HC, C-27 and BGC-823. The cells with highest expression of TROP-2 were transfected with different doses of TROP-2 siRNA. The expression of TROP-2 mRNA and protein was detected by real-time quantitative PCR and immumoflureseence method. Cell adhesion, migration,and invasion were exmined by hoyden chamber, respectively. Results Cell line BGC-823 showed the highest elevation of TROP-2 mRNA among three gastric cancer cell lines. Real-time quantitative PCR and immumoflurescence method revealed that the expression of TROP-2 mRNA and protein was reduced in a time- and dose-dependent manner ( r = 0. 935 ; r = 0. 922). The ability of adhesion, migration and invasion of BGC-823 cells treated with TROP-2 siRNA was decreased as compared with control group (P <0. 01 ). Conclusion TROP-2 gene might play an important role in adhesion, migration, and invasion of human gastric cancer cells, siRNA targeted TROP-2 could effectively inhibit adhesion, migration, and invasion of human gastric cancer cells. Key words: Gastric carcinoma; TROP-2; RNA interference; Invasion