Regulatory effect of siRNA interference targeting BMI-1 gene on proliferation of bladder cancer EJ cells

AIM: To investigate whether siRNA-mediated BMI-1 gene silencing inhibits the proliferation of EJ cells by detecting the expression of BMI-1, p16^INK4a and p14^ARF genes at mRNA and protein levels in bladder cancer EJ cells and normal bladder transitional epithelium cells. METHODS: The protein expression and localization of BMI-1, p16^INK4a and p14^ARF in EJ cells were determined by cellular immunofluorescence. An siRNA targeting BMI-1 gene was synthesized and transfected into bladder carcinoma EJ cells by liposomes. The mRNA expression of BMI-1, p16^INK4a and p14^ARF was detected by real-time PCR and the protein levels were measured by Western blotting in bladder cancer EJ cells and normal bladder transitional epithelium cells. Cell survival was analyzed by CCK-8 assay. Cell apoptosis were examined by flow cytometry. RESULTS: The mRNA and protein expression of BMI-1 in EJ cells was higher than that in bladder transitional epithelium cells. However, the expression of p16^INK4a and p14^ARF were opposite.While BMI-1 gene in EJ cells was silenced by siRNA, the mRNA and protein expression of BMI-1 were declined whereas the expression of p16^INK4a and p14^ARF was increased. The viability of the EJ cells was decreased and the apoptotic cells were increased when BMI-1 gene was silenced. CONCLUSION: The expression of BMI-1 is inversely correlated with the expression of p16^INK4a and p14^ARF in bladder transitional cell carcinoma EJ cells. The siRNA-mediated BMI-1 gene silencing in bladder cancer EJ cells inhibits the cell growth and up-regulates the expression of p16^INK4a and p14^ARF in vitro.     

Association between methylation status of apoptosis-related genes and chemosensitivity of lung adenocarcinoma cell line P15

AIM: To investigate the association between methylation status of apoptosis-related genes and chemosensitivity in the lung adenocarcinoma cell line P15.METHODS: Methylation-specific PCR was applied to detect the methylation status of p73, p14^ARF, p16^INK4a and bax genes of P15 cells in untreated control group and decitabine (DAC) treatment group. RT-PCR was used to detect the expression of p73, bcl-xL, bad, bax, p14^ARF and p16^INK4a at mRNA level. Colony formation assay and cell growth inhibition assay were used to detect the sensitivity of P15 cells to cis-diaminedichloroplatinum (C-DDP) before and after DAC treatment. DAPI staining was used to determine the apoptosis of P15 cells exposed to C-DDP before and after DAC treatment. RESULTS: p73, p16^INK4a and bax were expressed in the methylation status. After DAC treatment, p16^INK4a expression was decreased, and the expression of p73 and bax disappeared. The expression of p73, p16^INK4a and bax in the unmethylated status was weak, but the enhanced expression was observed following DAC treatment. After P15 cells were treated with DAC and C-DDP, the colony formation rate of the P15 cells was significantly decreased as compared with untreated control group. The apoptotic P15 cells in DAC+C-DDP treatment group were significantly higher than those in untreated control group (P<0.05). CONCLUSION: After treated with DAC, the sensitivity of P15 cells to C-DDP is increased due to the activation of silenced pro-apoptotic genes. DAC and C-DDP synergistically promote tumor cell apoptosis. They have significant anti-tumor effect.     

Correlation between hypermethylation and expression of Syk gene in colorectal cancer cell lines

AIM:To explore the relationship of methylation status and expression of spleen tyrosine kinase (Syk) gene in colorectal cancer cell lines. METHODS:Bisulfite sodium modification sequencing, methylation specific PCR and Western blotting were used to detect the methylation status and expression of Syk gene in 23 colorectal cancer (CRC) cell lines. Luciferase assay was applied to measure the activity of promoter with or without methylation in CpG islands. Meanwhile, methylation status and expression level were compared in Syk(-) HCT-15 cell line before or after 5-Aza-CdR administration. RESULTS:(1) Among 23 cell lines, loss expression of Syk gene in 9 cell lines due to hypermethylation in promoter, and 14 expression with unmethylation status were observed. The total methylation rate was 39.2%. (2) Microsatellite instability was found in 7 of 9 cell lines with promoter hypermethylation, 4 of 14 were wihtout hypermethylation. The difference between methylation and unmethylation group was significant (P<0.05). (3) 5-Aza-CdR restored methylated-Syk gene promoter activity. Compared to methylated-promoter, luciferase activities increased to 4.5 and 4.7 folds with Syk full size promoter and unmethylated-promoter, respectively. (4) 5-Aza-CdR restored methylated-Syk gene expression and the effect had time-course dependence. CONCLUSION:Hypermethylation of CpG islands in Syk gene promoter silences Syk expression in CRC cell lines, and 5-Aza-CdR restores Syk expression by demethylation.     

Analysis of p16 gene deletion and mutation in gastric carcinoma

AIM:To investigate p16 gene alterations in gastric carcinoma. METHODS:36 fresh tumor specimens taken from gastric cancer patients were analyzed for p16 gene deletion and mutation by polymerase chain reaction (PCR) and DNA sequencing. RESULTS:Homozygous deletion of exon 1 and exon 3 was observed in 2 cases and 3 cases of diffuse carcinoma, respectively. The frequency of homozygous deletion was 13.89%. No p16 gene point mutation was detected. CONCLUSION:The deletion of p16 genes may be related to gastric carcinogenesis.     

Hypermethylation of SFRP genes in esophageal squamous cell cancer

AIM: To investigate the promoter methylation of secreted frizzled-related protein(SFRP) genes in esophageal squamous cell cancer(ESCC). METHODS: The methods of methylation-specific PCR(MS-PCR) and RT-PCR were applied to examine the CpG methylation of the SFRP promoter and the mRNA expression of SFRP genes,respectively, in 78 samples of ESCC and corresponding adjacent non-cancer tissues. The protein expression of β-catenin was determined by immunohistochemistry.RESULTS: In the ESCC tissues, the frequencies of promoter methylation in SFRP1 , SFRP2 , SFRP4 and SFRP5 genes were 65.4%(51/78), 69.2%(54/78), 62.8%(49/78) and 52.6%(41/78),respectively, significantly higher than those in the adjacent tissues(P<0.01). The hypermethylation of these genes had no correlation with clinical stage and pathological classification in ESCC tissues(P>0.05). The frequency of simultaneous methylation of the 4 genes was correlated with the clinical stage(P<0.05). The positive rates of mRNA expression of the 4 genes in ESCC tissues were 42.3%(33/78), 46.2%(36/78), 50.0%(39/78) and 39.7%(31/78), respectively lower than those in the adjacent tissues(P<0.01). The mRNA expression of SFRP genes and the ectopic expression of β-catenin were correlated with the methylation frequency of SFRP genes(P<0.01).CONCLUSION: Promoter methylation of SFRP1 , SFRP2 , SFRP4 and SFRP5 genes was a frequent event in ESCC, indicating a contribution to the pathogenesis of ESCC through aberrant canonical Wnt/β-catenin signaling pathway. Combination analysis of methylation status in SFRP genes may has definite value on estimating prognosis of ESCC.     

Expression of natural killer cell stimulatory receptor NKG2D and its ligand MICA in Tibetan patients with gastric cancer at Qinghai plateau

AIM: To investigate the expression of natural killer cell stimulation receptor D(NKG2D) in peripheral blood and the expression of major histocompatibility complex class I chain-related protein A(MICA) on the gastric carcinoma tissue and the neighboring non-cancerous tissue in Tibetan patients with gastric cancer at Qinghai plateau. METHODS: Samples of 33 patients and 20 healthy persons were collected to detect NKG2D in peripheral blood by Flow cytometry analysis. The expressions of MICA in part of the correspondent tissues were examined by RT-PCR and immunohistochemistry.RESULTS: The expression of NKG2D in the plateau of Tibetan patients with gastric cancer group (13.47 ±5.26)% was significantly lower than that in healthy groups (32.62±10.08)%. The mRNA level of MICA in gastric cancer was significantly higher than that in neighboring non-cancerous tissue (P<0.05). The expressions of MICA proteins showed a significant difference between the neighboring non-cancerous tissue (21.21%, 7/33) and the gastric carcinoma tissue (78.79%, 26/33), between the high differentiation (60.00%, 3/5) and the moderate (72.73%, 8/11), low differentiation (88.24%, 15/17). The expressions of MICA were not correlated with tumor size, sex, age, lymph node metastasis of the patients (P>0.05). Spearman rank correlation displayed that the expressions of MICA mRNA were positively correlated with the MICA protein level (r=0.903, P<0.01).CONCLUSION: The immune escape in Tibetan patients with gastric cancer at Qinghai plateau probably relates to the down-regulation of NKG2D and the up-regulation of its ligand MICA. The activity of NK cells and the anti-cancer cellular immunity level are descending in the plateau of Tibetan patients with gastric cancer. The decrease in the receptor NKG2D is a reason for the activity of NK cell descending.     

Detection of bcl-2 methylation and the relationship between bcl-2 methylation and expression,prognostic factors in breast cancer

AIM: To establish methylation-specific PCR (MSP) method for detecting bcl-2 gene, and to study the relationship between bcl-2 methylation and expression, prognostic factors in breast cancer. METHODS: The primer of bcl-2 gene for MSP was designed. The methylations in CpG island of bcl-2 gene in 54 cases of breast cancer were detected by using MSP. The expressions of bcl-2, PCNA, ER and PR in 54 cases of breast cancer were detected by using SP immunohistochemical technique. RESULTS: The overall positive rate of bcl-2 methylation was 29.6% in breast cancer. There was a significant negative correlation between the methylation of bcl-2 and the expression of bcl-2 (P＜0.01). The methylation of bcl-2 coincided with those bad prognostic factors such as high PCNA label index (LI), ER-and PR-(P＜0.01). CONCLUSIONS: This study established the MSP method for detecting bcl-2 gene. The results of MSP and sequence analysis testified that the design of the MSP primer of bcl-2 gene in this study was successful. The methylation of bcl-2 would become the marker indicating bad prognosis of breast cancer.     

Differential expression of Golgi mannosidaseⅡ in different differentiated gastric carcinoma cell lines and tissues

AIM: To explore the role of Golgi mannosidase Ⅱ(GMⅡ) in the development of gastric carcinoma by analysis of the relationship between differential expression of GMⅡ and differentiation of gastric carcinoma cell lines and tissues. METHODS: Thirty cases of human normal gastric tissues and 38 cases of gastric adenocarcinoma tissues were selected. Three different differentiated gastric carcinoma cell lines (MKN-28, SGC-7901 and BGC-823) and a normal gastric epithelial cell line GES-1 were cultured in vitro. The mRNA levels of GMⅡ were detected by RT-PCR, and the protein expression was detected by immunohistochemistry and Western blotting. RESULTS: GMⅡ was mainly distributed in cytoplasm. The positive rates of GMⅡ in 30 cases of human normal gastric tissues, 8 cases of well-differentiated, 18 cases of moderately-differentiated and 12 cases of poorly-differentiated gastric cancer tissues were 53% (16/30), 63% (5/8), 83% (15/18) and 100% (12/12), respectively. The expression of GMⅡ was gradually increased in normal gastric epithelial cell line and in well, moderately and poorly-differentiated gastric cancer cell lines by cell-attached coverslip. Compared with normal gastric epithelial cell line, 3 gastric carcinoma cell lines showed the higher expression of GMⅡ at mRNA and protein levels (P<0.05). Furthermore, GMⅡ expression in poorly-differentiated gastric carcinoma cell line BGC823 was the highest, and the lowest expression of GMⅡ was the well-differentiated cell line MKN-28. Compared with normal gastric epithelial tissues, gastric carcinoma tissues showed the higher expression of GMⅡ at mRNA and protein levels (P<0.05), and the highest was the poorly-differentiated carcinoma tissues. The expression of GMⅡ at mRNA and protein levels in normal gastric tissues was the lowest. CONCLUSION: GMⅡ is involved in the development and progression of gastric cancer. The expression of GMⅡ is highly related to the poorly-differentiated gastric cancer.     

Methylation of TIMP-3 gene and their relationships with their clinical-pathological characteristics of colorectal cancers

AIM: To investigate whether methylation of the TIMP-3 gene is associated with clinical-pathological characteristics, recurrence and metastasis of the colorectal cancer. METHODS: Nest methylation specific PCR (nMSP) and RT-PCR techniques were used to detect methylation of TIMP-3 gene and its mRNA expression in the colorectal cancer specimen and adjacent non-cancerous tissues. RESULTS: The expression of TIMP-3 mRNA in tumor tissues was distinctly reduced (P<0.01). The expression of TIMP-3 mRNA in those without lymph node metastasis was higher than those with lymph node metastasis (P<0.01). The patients with Duke's C, D and lymph node metastasis were more to contain methylated TIMP-3 compared to those with Duke's A, B and no lymph node metastasis (P<0.05). Statistical differences in pathological characteristics such as tumor site, Duke's stage, histological differentiation and type between TIMP-3 methylation positive group and negative group were observed (P<0.05). CONCLUSION: Methylation of the TIMP-3 gene promoter usually occurs in the proximal site, infiltrating type, poor cellular differentiation, lymph node metastasis and advanced stage of colorectal cancers patients.     

Effect of cell cycle regulator p21WAF1 on hypertrophy of peritoneal mesothelial cells

AIM: To investigate the effect of cell cycle regulator p231^WAF1 on hypertrophy of peritoneal mesothelial cells affected by high concentrated glucose. METHODS: RT-PCR and Western Blot method were used to detect p21^WAF1 expression of rat peritoneal mesothelial cells in high glucose concentration medium (containing 1.86%, 3.86% glucose) after 24 hours. Flow cytometer technique was used to analyze the cell cycle distribution. RESULTS: In high glucose medium, most of the cells became hypertrophy, and were arrested in G1 phase of the cell cycle, which was obvious in 3.86% glucose group. Glucose increased p21 mRNA and protein expression in a dose-dependent manner, and the levels of p21^WAF1 mRNA and protein in 3.86% glucose group were higher than those in 1.38% glucose group (P＜0.05). p21 ^WAF1 mRNA and protein expression were absent in the serum-free normal medium and D-mannitol groups which had the same osmolarity as the glucose groups. CONCLUSION: p21^WAF1 may be pivotal in the hypertrophy and arrest in the G1 phase of mesothelial cells induced by high concentrated glucose.     

Application of multiple gene methylations in plasma for diagnosis of lung cancer

AIM: To determine the aberrant methylation status in the gene promoter regions of CDH13, RASSF1A, DLEC1, SEPT9and RUNX3by detecting the plasma specimens and the value of their combined detection for diagnosis of lung cancers. METHODS: Nest methylation specific PCR (nMSP) was used to detect the promoter methylation status of the 5 genes in the plasma from 106 normal controls， lung cancer tissues, lung benign tissues and the plasma from 106 patients with lung cancers. Multiple displacement amplification (MDA) was used to amplify modified genomic DNA to solve the problem of insufficient of plasma DNA template. RESULTS: The positive rates of promoter methylation of CDH13, RASSF1A, DLEC1, SEPT9and RUNX3in the lung cancer tissues were 51.9%, 44.3%, 54.7%, 36.8%, 24.5%, respectively, and those in the plasma were 46.2%, 41.5%, 50.9%, 31.1%, 19.8%, respectively. The results of the Kappa consistency check showed that the lung cancer tissues and the plasma had obviously coherence in the methylation status of the 5 gene promoter regions. Combination of DLEC1, CDH13, RASSF1A, and SEPT9 had a higher diagnostic efficiency than the others, as their ACC value was 0.8208 and youden index was 0.6415 (with the sensitivity of 81.13% and the specificity of 83.02%). CONCLUSION: Combination detection of promoter methylation of lung cancer-related genes in the plasma is expected to apply to the early diagnosis of lung cancer.     

Expression of Foxp3+ Tregs and PD1 in gastric cancer tissues and their correlation with clinicopathological factors and prognosis

AIM: To investigate the expression of Foxp3⁺ regulatory T cells (Foxp3⁺ Tregs) and programmed death receptor 1 (PD1) in gastric cancer tissues and their association with clinicopathological factors and prognosis of the patients. The correlation between the 2 molecules was also analyzed at the same time. METHODS: The tumor sections from 111 gastric cancer patients were stained for Foxp3 and PD1 by the method of immunohistochemistry. The associations of the expression levels of these 2 molecules with clinicopathological factors involved in the disease progression and prognosis were statistically analyzed. The relationship of their expression was detected. RESULTS: Foxp3⁺ Tregs and PD1 were expressed in the gastric cancer tissues, and PD1 was expressed in the tumor infiltrating lymphocytes (TILs). The expression of Foxp3 and PD1 was correlated with lymph node metastasis, clinicopathological stage and prognosis of gastric cancer patients. The expression of these 2 determinants in the patients with lymph node metastasis and an advanced clinicopathological stage was distinctly higher (P <0.05). The patients with positive expression of the 2 indexes presented a lower overall survival rate and worse prognosis (P <0.05). A significantly positive correlation between the infiltration of Foxp3⁺ Tregs and the expression of PD1⁺ TILs was also observed (P <0.01).CONCLUSION: Foxp3⁺ Tregs and PD1⁺ TILs co-infiltrate in the gastric cancer tissues, which can be used as biological markers to predict the disease progression and prognosis.     

Clinical significance of detection of p16 gene methylation in early diagnosis of lung cancer

AIM: To investigate the aberrant methylation in the promoter of p16 in plasma, sputum, bronchoalveolar lavage fluid (BALF), pleural effusion and biopsy specimens from suspected lung cancer patients and to evaluate the clinical significance in the early diagnosis of lung cancer.METHODS: Using methylation specific PCR (MSP) for the detection of promoter methylation of p16 gene in plasma, sputum, BALF, pleural effusion and biopsy specimens from suspected lung cancer patients.RESULTS: Of the 67 cases of suspected lung cancer patients, 42 were proved by pathology. The positive percentages of p16 gene promoter methylation of the lung cancer patients are as follows: 52.4%（22/42）in plasma, 47.6%（20/42）in sputum, 59.5%（25/42）in BALF, 71.4%（10/14）in pleural effusion and 61.9%（26/42）in biopsy specimens, respectively；while promoter methylation in p16 gene was found only one in plasma and one in pleural effusion in 25 patients with various benign lesions (P<0.05). The positive expression of p16 gene promoter methylation in lung cancer patients was irrelevant to histological type, clinical stage, pathological grade, lymph node metastasis and distant metastasis of the lung carcinomas (P>0.05).CONCLUSION: Detection of the aberrant methylation in the promoter of p16 gene in plasma, sputum, BALF, pleural effusion and biopsy specimens from lung cancer patients by MSP method is a kind of rising technology with development potential for lung cancer early diagnosis.     

Effect of DNA methylation of miR-30a-5p promoter region on hepatic injury induced by homocysteine

AIM: To explore the role of DNA methylation of microRNA-30a-5p(miR-30a-5p) promoter region in hepatic injury. METHODS: Four-week-old normal mice and cystathionine β-synthase (CBS) single gene knockout mice were used and divided into normal (CBS^+/+, n=12) group and single gene knockout (CBS^+/-, n=12) group, and the mice were fed with high methionine diet for 8 weeks. HL-7702 hepatic cells were routinely cultured in vitro and divided into control group, homocysteine (Hcy) group and Hcy+5-azacytidne (AZC) group. Serum Hcy, alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels were measured by automatic biochemical analyzer. The levels of ALT and AST in the cells culture medium were determined by the microplate method. Hepatic injury in the mice were observed with HE staining. Cell viability staining was used to measure the viability of hepatocytes. RT-qPCR was used to detect the expression of miR-30a-5p in the liver tissues and hepatocytes. The correlation between the expression of miR-30a-5p and serum ALT and AST levels was analyzed by Pearson correlation analysis. DNA methylation level of miR-30a-5p promoter region in the liver tissues and hepatocytes was detected by nested landing methylation-specific PCR (nMS-PCR). RESULTS: Compared with the CBS^+/+ mice, the serum levels of Hcy, ALT and AST in the CBS^+/- mice were significantly increased (P < 0.05). HE staining showed the hepatocyte swelling and nuclear fragmentation and dissolution. The expression level of miR-30a-5p in the liver tissues was decreased (P < 0.01). Besides, the expression level of miR-30a-5p in the mice was negatively correlated with serum ALT and AST levels (r²=0.4557, P=0.0003, r²=0.4626, P=0.0003), and the DNA methylation of miR-30a-5p promoter region was increased (P < 0.01). In the HL-7702 cells, compared with control group,the ALT and AST levels were increased in Hcy group (P < 0.05, P < 0.01), and the cell viability was remarkablely decreased. DNA methylation of miR-30a-5p promoter region was increased (P < 0.01), which decreased after treated the cells with AZC (P < 0.05), while the expression level of miR-30a-5p in the cells was increased (P < 0.05). CONCLUSION: Hypermethylation of miR-30a-5p promoter region may play an important role in hepatic injury.     

Methylation and mRNA expression of TIG1 gene in esophageal squamous-cell carcinoma tissues

AIM: To investigate the expression and promoter methylation of tazarotene-induced gene-1 (TIG1) in esophageal squamous-cell carcinoma (ESCC) tissues. METHODS: The methods of methylation-specific PCR and real-time fluorescence quantitative PCR were applied to examine the methylation and mRNA expression of TIG1, respectively, in 43 cases of ESCC tissues, 20 cases of paracancerous tissues and 15 cases of normal tissues. RESULTS: The frequency of promoter methylation of TIG1 gene in ESCC tissues was 25.6% (11/43), which was significantly higher than that in the paracancerous tissues (5.0%, 1/20) and normal tissues (0/20). The hypermethylation of TIG1 gene in these tissues had no correlation with sex, age and clinical stage of the patients. However, it was correlated with the pathological stage (P<0.01) and lymph node metastasis (P<0.05). The mRNA expression of TIG1 in ESCC tissues was significantly lower than that in paracancerous tissues (P<0.05) and normal tissues (P<0.01). However, the expression level of TIG1 mRNA in methylated tissues was significantly lower than that in unmethylated tissues (P<0.01). CONCLUSION: Promoter methylation may be an important mechanism of TIG1 gene inactivation in ESCC, which was related to lymph node metastasis and TNM stage of esophageal carcinoma.     

Study on hyper methylation of p15INK4B gene in multiple myeloma

AIM: To study the characteristics and regulations of p15 (MST INK4B) methylation in multiple myeloma (MM). METHODS: Method of methylation-specific PCR was applied in 23 cases of MM about the methylation rate of p15 gene. RESULTS: Methyaltion rate in MM was 73.5%(17/23). The PCR product was a fragment of 148 bp. In four stageⅠcases of MM with plasma cell-typed bone marrow profile, p15^INK4B gene was non-methylated; In one case of stag ⅡMM and one case of stage Ⅲ MM with mature plasma typed bone marrow profile, p15^INK4B gene was no-methylated, too, while in many cases of stageⅠ、stage Ⅱand stage Ⅲ with naive plasma cell in bone marrow profile which were plasma cell-typed or mixed typed, p15^INK4B gene methylation was frequently detected. The methylation rates for stageⅠ、stage Ⅱand stage Ⅲ MM were respectively 55%(5/9),100%(7/7) and 71.4%(5/7). CONCLUSION: p15 gene methylation was a possible pathogenic factor,and might be related to the progression and prognosis of the disease.     

Effect of CD97 gene silencing by small interfering RNA on migration and invasion of gastric carcinoma cell lines

AIM: To investigate the effect of CD97 gene silencing by small interfering RNA(siRNA) on migration and invasion of gastric carcinoma cell lines. METHODS: Gastric carcinoma cell lines AGS and MGC803 were used in the study. Four pairs of siRNA were designed according to the sequence of CD97 gene and synthesized chemically. The siRNAs were transfected into the gastric carcinoma cell lines. Forty-eight hours after transfection, the total RNA was extracted and the mRNA expression of CD97 was detected by real-time RT-PCR so as to screen the most effective siRNA. The protein level of CD97 was also measured by fluorescence-activated cell sorting (FACS) 72 h after Transfection. The abilities of migration and invasion were evaluated by Transwell test. The viability of the cells was measured by MTT method. RESULTS: Real-time RT-PCR and FACS revealed that CD97-siRNA notably down-regulated CD97 expression at both mRNA and protein levels. The mRNA level decreased by (89.34±9.95)% and (95.42±1.93)% in AGS and MGC803 cells,respectively. The protein levels of CD97^EGF and CD97^stalk in AGS cells decreased by (19.29±3.45)% and (30.11±5.93)%,respectively. The protein levels of CD97^EGF and CD97^stalk in MGC803 cells decreased by (26.25±5.73)% and (16.22±3.23)%,respectively. No change of the cell viability after siRNA transfection was observed. The cell number of migration and invasion in AGS cells was decreased by (67.63±12.03)% and (68.02±15.63)%,respectively. The cell number of migration and invasion in MGC803 cells was decreased by (14.92±2.03)% and (22.09±5.43)%,respectively. CONCLUSION: The siRNA effectively inhibits CD97 expression and restrains the migration and invasion capacities of gastric carcinoma cell lines, suggesting that CD97 plays an important role in the metastasis of gastric cancer.