Human Gastric Cancer SGC-7901 Cells Research Articles

Chemopreventive Effects of Peucedanum praeruptorum DUNN and Its Major Constituents on SGC7901 Gastric Cancer Cells

In this study, the effects of Peucedanum praeruptorum DUNN methanolic extract (PPME) and its major constituents on SGC7901 human gastric cancer cells were evaluated. Two pyranocoumarins, namely, (±) praeruptorin A (PA) and (±) praeruptorin B (PB), were isolated from PPME. A high performance liquid chromatographic (HPLC) method was developed to determine the contents of PA and PB in PPME. The anti-proliferative and cytotoxic actions of PPME were observed using the 3-(4,5-dimethyl-thiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and release of lactate dehydrogenase (LDH) assays. At 300 μg/mL, PPME inhibited cell growth by 51.2% (P < 0.01), probably linked to the high concentration of PA and PB. Both PA and PB exhibited antiproliferative and cytotoxic activities on the SGC7901 cells. Furthermore, the active principle compound, PA, also enhanced the actions of doxorubincin (DOX) on SGC7901 cells. Cell growth decreased higher with the combined treatment of PA and DOX than that with the chemotherapy agent applied alone, suggesting that PA could reduce the dose of DOX for the desired effects.

Novel 3-(1-acetyl-5-(substituted-phenyl)-4,5-dihydro-1H-pyrazol-3-yl)-7-fluoro-2H-chromen-2-one Derivatives: Synthesis and Anticancer Activity

A series of novel coumarin derivatives containing 4,5-dihydropyrazole moiety as potential telomerase inhibitors were synthesized. The bioassay tests showed that compound 3b exhibited potentially high activity against human gastric cancer cell SGC-7901 with IC50 value was 2.98±0.16. Docking simulation was performed to position compound 3b into the telomerase (3DU6) active site to determine the probable binding model. The result shows that some coumarin containing 4,5-dihydropyrazole moiety can combine well with the telomerase active site and may have use as potential telomerase inhibitors.

Activation of RASSF2A by p300 induces late apoptosis through histone hyperacetylation

Both RASSF2A (Ras-associated family 2A) and p300 are implicated in apoptosis. However, little is known about the interrelationship between these two proteins in induction of apoptosis. Here we show that p300 was able to induce late apoptosis through up-regulation of RASSF2A in human gastric cancer cells SGC-7901 (p53-mutant). Our data demonstrated that p300 stimulated RASSF2A expression in 293T cells in cooperation with the transcription factor Sp1. Results of ChIP (chromatin immunoprecipitation) assays revealed that p300 induced histones H3 and H4 hyperacetylation at RASSF2A promoter. Moreover, p300 and Sp1 reciprocally facilitated their binding to RASSF2A promoter. Overall, data arising from this study indicate that Sp1-mediated RASSF2A gene transcription is activated by p300 through histone acetylation, and this activation plays an important role in inducing late apoptosis.

Inhibition of tankyrase 1 in human gastric cancer cells enhances telomere shortening by telomerase inhibitors

Telomere stability is believed to be related to aging and tumorigenesis. Besides telomerase, telomere length is also regulated by several telomere-specific binding proteins. Tankyrase 1, a telomeric poly(ADP-ribose) polymerase (PARP), elongates telomere length by inhibiting TRF1 binding to telomeres. In order to study the synergistic action of tankyrase 1 and telomerase in the maintenance of telomere length in mammalian cells, we constructed anti-sense tankyrase 1 (aTNKS) eukaryotic expression vectors and then transfected them into the SGC-7901 human gastric cancer cell line, as well as SGC-7901 cells that had been transfected with antisense hTR (7901-ahTR) and antisense hTERT (7901-ahTERT) with DOTAP liposomes. The activity of telomerase, telomere length and telomerase-associated protein activities were measure by TRAP-ELISA, Southern blot and western blot analysis, respectively, in aTNKS transfected and untransfected cells. The results demonstrated that telomere length was significantly shorter in cells with concomitant tankyrase 1 and telomerase inhibition than by either tankyrase 1 or telomerase inhibition alone, in SGC-7901 cells. We also found that aTNKS had no effect on telomerase activity. These results reveal that inhibition of tankyrase 1 could shorten telomere length and play a synergistic role with telomerase inhibitors in telomere length shortening in the SGC-7901 gastric cancer cell line. Co-inhibition of tankyrase 1 and telomerase activity may be a rational strategy for telomere-directed gastric cancer therapeutics.

Inhibition of tankyrase 1 in human gastric cancer cells enhances telomere shortening by telomerase inhibitors

Telomere stability is believed to be related to aging and tumorigenesis. Besides telomerase, telomere length is also regulated by several telomere-specific binding proteins. Tankyrase 1, a telomeric poly(ADP-ribose) polymerase (PARP), elongates telomere length by inhibiting TRF1 binding to telomeres. In order to study the synergistic action of tankyrase 1 and telomerase in the maintenance of telomere length in mammalian cells, we constructed anti-sense tankyrase 1 (aTNKS) eukaryotic expression vectors and then transfected them into the SGC-7901 human gastric cancer cell line, as well as SGC-7901 cells that had been transfected with antisense hTR (7901-ahTR) and antisense hTERT (7901-ahTERT) with DOTAP liposomes. The activity of telomerase, telomere length and telomerase-associated protein activities were measure by TRAP-ELISA, Southern blot and western blot analysis, respectively, in aTNKS transfected and untransfected cells. The results demonstrated that telomere length was significantly shorter in cells with concomitant tankyrase 1 and telomerase inhibition than by either tankyrase 1 or telomerase inhibition alone, in SGC-7901 cells. We also found that aTNKS had no effect on telomerase activity. These results reveal that inhibition of tankyrase 1 could shorten telomere length and play a synergistic role with telomerase inhibitors in telomere length shortening in the SGC-7901 gastric cancer cell line. Co-inhibition of tankyrase 1 and telomerase activity may be a rational strategy for telomere-directed gastric cancer therapeutics.

Synthesis and cytotoxicity of novel chrysin derivatives

A series of chrysin derivatives 8a–8v were prepared and tested in vitro against HCT-116 (human colon cancer cell line), Hela (human cervical carcinoma cell line), DU-145 (human prostate cell line), K562 (human leukemia cell line), and SGC-7901 (human gastric cancer cell line). The chemical structures of these compounds were confirmed by means of MS, IR, 1H NMR, 13C NMR, and elemental analysis. Among these derivatives, 7-(2-(piperazin-1-yl)ethoxy)-5-hydroxy-2-phenyl-4H-chromen-4-one, 8n, had the strongest activity against HCT-116, Hela, DU-145, K562, and SGC-7901 cells.Open image in new window .

Synthesis and molecular docking study of novel coumarin derivatives containing 4,5-dihydropyrazole moiety as potential antitumor agents

A series of novel coumarin derivatives containing 4,5-dihydropyrazole moiety as potential telomerase inhibitors were synthesized. The bioassay tests show that compound 3d exhibited potentially high activity against human gastric cancer cell SGC-7901 with IC 50 value of 2.69 ± 0.60 μg/mL. All title compounds were assayed for telomerase inhibition by a modified TRAP assay, the results show that compounds 3d and 3f can strongly inhibit telomerase with IC 50 values of 2.0 ± 0.07 and 1.8 ± 0.35 μM, respectively. Docking simulation was performed to position compound 3d into the telomerase (3DU6) active site to determine the probable binding model.

Cytotoxic Pentacyclic Triterpenoids from Combretum oliviforme

Four pentacyclic triterpenoids were obtained from the leaves of Combretum oliviforme Chao, 3beta-hydroxyolean-12-en-28-oic acid (1), 23-O-[alpha-L-(4'-acetylrhamnopyranosyl)]-imberbic acid (2), 23-acetoxy-3beta-acetylimberbic acid-29-methyl ester (3), and 23-O-[alpha-L-rhamnopyranosyl]-1,3beta-diacetylimberbic acid (4). Hydrolysis of 2 and 4 gave 23-hydroxyimberbic acid (5). The structures were elucidated by NMR, electrospray ionization mass spectrometry (ESIMS) and comparison with literature data. Compounds 1, 2, 3 and 4 were isolated from C. oliviforme Chao leaves for the first time and 3 for the first time from any natural source. All compounds were tested in vitro for their activity against human lung cancer cell line SPC-A-1, human erythroleukaemic line K562 and human gastric cancer SGC-7901 cells. Compounds 1, 3, 4 and 5 had cytotoxic activity for the three cell lines with IC50 0.69-69.68 microM. These results suggest that the presence of acetyl group in the triterpene aglycone structure plays an essential role for cytotoxic activity.

Critical role of aquaporin-3 in the human epidermal growth factor-induced migration and proliferation in the human gastric adenocarcinoma cells

Background: Aquaporins (AQPs) are expressed in many different tumor cell types in human. New evidence for the involvement of AQPs in cell migration and proliferation adds AQPs to an expanding list of effectors in tumor biology.Aims: The aim of this study was to investigate whether AQP3 expression in the human gastric carcinoma cell lines, AGS and SGC7901, enhances cell migration and proliferation. Methods: Cultured AGS or SGC7901 cells were treated with human epidermal growth factor (hEGF) and subjected to cell migration assay and cell proliferation assay. The expression or activation level of proteins was analyzed by western blot. AQP3 knockdown was obtained by small interfering (si) RNA.Results: Here, we showed that AQP3 is expressed in the human gastric cancer cell lines, AGS and SGC7901. The hEGF induced AQP3 expression in a time- and dose-dependent manner and increased gastric cancer cell migration and proliferation. AQP3 knockdown by siRNA inhibited hEGF-induced AQP3 expression and thus cell migration and proliferation. Furthermore, a mitogen-activated protein kinase (MEK)/extracellular signal-regulated kinase (ERK) inhibitor U0126 inhibited hEGF-induced AQP3 expression and cell migration or proliferation. Conclusions: Collectively, our findings provide for the first time that AQP3 plays a critical role in hEGF-induced cancer cell migration and proliferation and that hEGF induces AQP3 expression via ERK signal transduction pathways. These finds provide evidence for a novel role of AQP3 in human gastric carcinoma as a potentially important determinant of tumor growth and spread.

RNAi-mediated silencing of CD147 inhibits tumor cell proliferation, invasion and increases chemosensitivity to cisplatin in SGC7901 cells in vitro

BackgroundCD147 is a widely distributed cell surface glycoprotein that belongs to the Ig superfamily. CD147 has been implicated in numerous physiological and pathological activities. Enriched on the surface of many tumor cells, CD147 promotes tumor growth, invasion, metastasis and angiogenesis and confers resistance to some chemotherapeutic drugs. In this study, we investigated the possible role of CD147 in the progression of gastric cancer.MethodsShort hairpin RNA (shRNA) expressing vectors targeting CD147 were constructed and transfected into human gastric cancer cells SGC7901 and CD147 expression was monitored by quantitative realtime RT-PCR and Western blot. Cell proliferation, the activities of MMP-2 and MMP-9, the invasive potential and chemosensitivity to cisplatin of SGC7901 cells were determined by MTT, gelatin zymography, Transwell invasion assay and MTT, respectively.ResultsDown-regulation of CD147 by RNAi approach led to decreased cell proliferation, MMP-2 and MMP-9 activities and invasive potential of SGC7901 cells as well as increased chemosensitivity to cisplatin.ConclusionCD147 involves in proliferation, invasion and chemosensitivity of human gastric cancer cell line SGC7901, indicating that CD147 may be a promising therapeutic target for gastric cancer.

PEI-PEG as a siRNA genetic vector demonstrating interference in the expression of CD44v6 protein in gastric cancer cells

Objective To investigate the effect of polyethylene imine glycol (PEI-PEG)/siRNA nanocomposites in the in vitro transfection of human gastric cancer SGC7901 cell lines and the down-regulation of gene expression of the adherence factor CD44v6.

Upregulation of the GRIM-19 gene suppresses invasion and metastasis of human gastric cancer SGC-7901 cell line

Gene associated with retinoid-IFN-induced mortality 19 (GRIM-19), as a novel IFN-β/RA-inducible gene product, was identified as a potential tumor suppressor associated with growth inhibition and cell apoptosis. Recently, it has been reported that the apoptotic effects and apoptosis-related gene induction of GRIM-19 can be attenuated by GW112, indicating that GRIM-19 and GW112 are involved in a common signal transduction pathway. To investigate the signaling mechanisms that link GRIM-19 to GW112 and their functional role in tumor cell invasion and metastasis, we utilized adenovirus-mediated overexpression of GRIM-19 in the gastric cancer SGC-7901 cell line. We observed that enhanced expression of GRIM-19 not only downregulated GW112 but also decreased NF-кB binding activity. As a result, we found that tumor cell adhesion, migration, invasion and liver metastasis were inhibited. Additionally, upregulation of GRIM-19 also suppressed secretion of urokinase-type plasminogen activator (u-PA), matrix metalloproteinase (MMP)-2, 9 and vascular endothelial growth factor (VEGF). These results indicate that GRIM-19 acts as an upstream regulator of GW112 to block NF-кB binding activity, thereby inhibiting gastric cancer cell migration, invasion and metastasis. We conclude that adenoviral transfer of the GRIM-19 gene may be an efficacious approach to controlling the invasion and metastasis of human gastric cancer.

Endoplasmic reticulum stress contributes to vitamin E succinate-induced apoptosis in human gastric cancer SGC-7901 cells

Vitamin E succinate (RRR-α-tocopheryl succinate, VES), an efficient inducer of apoptosis, acts as a potent agent for cancer therapy. However, the mechanism by which VES mediates the effects are not yet fully understood. Here we studied the effect of endoplasmic reticulum (ER) stress and unfolded protein response (UPR) on VES-induced apoptosis of SGC-7901 human gastric cancer cells. VES caused cytological changes typical of apoptosis, increased ER dilation and cytosolic Ca 2+ concentration. And endogenous ER stress markers, GRP78 and GRP94 were transcriptionally and translationally altered. In response to VES, induction of CHOP, activation of caspase-4 and JNK were observed. Furthermore, VES also triggered activation of UPR components, including RNA-dependent protein kinase (PKR)-like ER kinase (PERK), activating transcription factor 6 (ATF6), X-box-binding protein 1 (XBP1), and ATF4 in a concentration- and time-dependent manner. Consequently, our results suggest that VES-induced apoptosis is coupled to ER stress and UPR activation in SGC-7901 human gastric cancer cells.

Anti-tumor Effects of Ampelopsin on Human Gastric Cancer SGC-7901 Implanted in Nude Mice

Objective To investigate the effects of ampelopsin(APS) on the growth of human gastric cancer cell SGC-7901 in nude mice.Methods SGC-7901 cells were inoculated into the nude mice to establish gastric cancer model.Then the BALB/C nude mice with xenograft tumor were randomized into 5 groups.The ampelopsin was administered at 3 dosages by irrigate the stomach daily for 10 d.The anti-tumor effects of ampelopsin was evaluated based on the tumor volume,relative tumor volume(RTV),tumor weight,relative tumor proliferative rate (T/C)and tumor inhibition rate(IR).Results At the 600mg/kg,300mg/kg,150mg/kg dose of APS,the relative tumor proliferation rate was 52.84%,71.12% and 62.14%,respectively,and the growth inhibition of the transplanted tumor was 38.8%,27.5% and 27.3%,respectively.Conclusion APS in appears to be a potent anti-tumor agent that was firstly discovered in the transplanted human gastric cancer cell SGC-7901 in nude mice in vivo.

Systemic and peritoneal inflammatory response after laparoscopic-assisted gastrectomy and the effect of inflammatory cytokines on adhesion of gastric cancer cells to peritoneal mesothelial cells

There still remain concerns over the potential for peritoneal metastasis after laparoscopic surgery. We designed this trial to investigate the effects of the inflammatory cytokines interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) on the interaction between gastric cancer cells and mesothelial cells, and to evaluate differences in both the peritoneal and systemic cytokine (IL-1β and TNF-α) concentrations after laparoscopic and conventional surgical approaches, thus offering another possible advantage of laparoscopic procedures for treatment of gastric cancer. A reproducible human in vitro assay was developed to study adhesion of SGC-7901 and MKN-45 human gastric cancer cells to monolayers of primary cultured human peritoneal mesothelial cells (HPMCs). Tumor cell adhesion to a mesothelial monolayer was assessed after preincubation of the monolayer with IL-1β and TNF-α using flow cytometry. Expression of adhesion molecules (ICAM-1, VCAM-1, and CD44) and their counterparts (LFA-1 and VLA-4) was investigated by real-time polymerase chain reaction (PCR) immunocytochemical staining. Furthermore, the proinflammatory cytokines IL-1β and TNF-α were measured perioperatively in peritoneal drain fluid and in serum by enzyme immunoassay. Preincubation of the mesothelial monolayer with IL-1β and TNF-α resulted in enhanced tumor cell adhesion of SGC-7901 and MKN-45 cells. Mesothelial cells showed significant enhancement of expression of ICAM-1, VCAM-1, and CD44 after stimulation with IL-1β and TNF-α. Meanwhile their counterparts (LFA-1, VLA-4, and CD44) were identified in gastric cancer cells. The level of IL-1β in peritoneal drain fluid and in serum perioperatively in the laparoscopy-assisted gastrectomy group was lower than in the conventional open gastrectomy group, whereas there were no significant differences between the laparoscopic-assisted distal gastrectomy (LADG) and conventional open distal gastrectomy(CODG) groups with respect to TNF-α. The presented results prove that IL-1β and TNF-α are significant stimulating factors in gastric cancer cell adhesion in vitro and may therefore partly account for local tumor recurrence and peritoneal metastasis in vivo. Owing to less impact on the postoperative abdominal regional and systemic immune responses, laparoscopic surgery not only shows clinically relevant advantages but also causes less effect of inflammatory factors on local recurrence and peritoneal metastasis of gastric cancer than conventional operations. Thus, we offer another possible advantage of laparoscopic procedures for treatment of gastric cancer.

The conformation change of Bcl-2 is involved in arsenic trioxide-induced apoptosis and inhibition of proliferation in SGC7901 human gastric cancer cells

BackgroundArsenic trioxide has been established as a first-line agent for treating acute promyelocytic leukemia. Experimental data suggest that arsenic trioxide also can have a potential use as chemotherapeutic agent for other malignancies. The precise mechanisms of action of arsenic trioxide have though not been elucidated. As the role of Bcl-2 in arsenic trioxide-mediated cell apoptosis and conformation change of Bcl-2 in response to arsenic trioxide treatment has not been studied. The aim of the present study was to determine whether conformation change of Bcl-2 is involved in the action of arsenic trioxide.MethodsHuman gastric cancer SGC7901 cells were exposed to different concentrations of arsenic trioxide. Proliferation was measured by using the Kit-8 cell counting assay. Analysis of nuclear morphology was observed by DAPI staining. The apoptosis rates of cells treated with arsenic trioxide were analyzed by flow cytometry using Annexin V-FITC staining. The conformation change of Bcl-2 and Bax activation were detected by immunostaining and Western blot analysis. Total expression of Bcl-2 and Bax were examined by Western blot analysis.ResultsArsenic trioxide inhibited the growth of human gastric cancer SGC7901 cells and induced apoptosis. There were two Bcl-2 phenotypes coexisting in SGC7901 cells and the Bcl-2 cytoprotective phenotype could change into a cytodestructive phenotype following conformational change of Bcl-2, triggered by arsenic trioxide exposure. Bax activation might also be involved in arsenic trioxide-induced Bcl-2 conformational change. Arsenic trioxide did not change levels of total Bcl-2 expression, but up-regulated total Bax expression for the treatment time ranging from 3 to 24 hours.ConclusionArsenic trioxide induces apoptosis through induction of Bcl-2 conformational change, Bax activation and up-regulation of total Bax expression rather than affecting total Bcl-2 expression in human gastric cancer SGC7901 cells. The conformational change of Bcl-2 may be a novel described mechanism of arsenic trioxide-induced apoptosis in cancer cells.

Cimetidine induces apoptosis in gastric cancer cells in vitro and inhibits tumor growth in vivo

Cimetidine, a histamine-2 (H2) receptor antagonist, has been demonstrated to have anticancer effects on various types of malignancies. However, the mechanisms of its action on gastric cancer are not completely understood. This study was designed to investigate its antitumor effect and underlying mechanisms in human gastric cancer SGC-7901 and MGC-803 cells. The MTT assay was used to evaluate cell viability, and flow cytometry, acridine orange staining and transmission electron microscopy were used to detect apoptosis, for cultured cells. The protein expression in cells was evaluated by Western blot analysis and colorimetric assay. Gastric tumors were established by subcutaneous injection of SGC-7901 cells in nude BALB/c mice, and cimetidine was administered to the mice. The size of tumors was monitored and the weight of tumors was examined. The exposure of gastric cancer cells to cimetidine resulted in growth inhibition and the induction of apoptosis in a dose-dependent manner. Activation of the caspase cascade for both the extrinsic and intrinsic pathways were demonstrated in vitro, including caspase-8, -9 and -3. We also found that the expression of Bcl-2 protein decreased and the expression of Bax protein increased which lead to an increase of the Bax/Bcl-2 ratio. In mice bearing SGC-7901 xenograft tumors, administration of cimetidine showed a significant decrease of tumor volumes and tumor weight compared with the control. Our results showed that cimetidine exhibited antitumor effects in gastric cancer cells with an induction of apoptosis.

Na+/H+ exchanger blockade inhibits the expression of vascular endothelial growth factor in SGC7901 cells

Vascular endothelial growth factor (VEGF) overexpression is critically involved in tumor formation. Na+/H+ exchanger isoform (NHE) is elevated in cancer cells. We explored the effect of NHE inhibition on VEGF expression in human gastric cancer SGC7901 cells. VEGF mRNA expression was detected by real-time RT-PCR. VEGF protein expression was measured by western blotting and immunocytochemistry. For determination of viable cells the MTT colorimetric assay was used. Treatment of SGC7901 cells with NHE inhibitors resulted in significant decrease of VEGF mRNA and protein expression. NHE inhibition decreased intracellular pH (pHi) values and VEGF mRNA expression. These data demonstrate that NHE blockade inhibits VEGF expression in SGC7901 cells.

RNAi‐mediated silencing of ezrin gene reverses malignant behavior of human gastric cancer cell line SGC‐7901

To investigate the effects of ezrin targeting gene of RNA interference (RNAi) on human gastric cancer cell line SGC-7901 in vitro. The highly metastatic human gastric cancer cell line SGC-7901 transfected with a small interfering (siRNA) lentivirus vector was selected for this research study. Expressions of ezrin mRNA and ezrin protein in the SGC-7901 cells were detected using RT-PCR and Western blot. Cell apoptosis was observed using flow cytometry. Transwell invasion and the cell adhesion test were used to verify the effect of RNAi on ezrin expression in the human gastric cancer cell line SGC-7901 in vitro. Ezrin gene targeting via a RNAi-mediated lentivirus vector had obvious inhibitory effects on ezrin expression in the human gastric cancer cell line SGC-7901. The results of the RT-PCR show the obvious inhibition of ezrin mRNA expression in Eai and Ebi groups (0.22 +/- 0.01 vs 0.95 +/- 0.04, P < 0.05; 0.31 +/- 0.01 vs. 0.95 +/- 0.04, P < 0.05). Western blot analysis revealed a 72.35 +/- 3.74% reduction of the ezrin protein level after interference with the ezrin targeting gene. Moreover, the inhibition of ezrin expression clearly inhibited SGC-7901 cell migration and invasion, and improved cell adhesion as well as increased sensitivity to camptothecin-induced apoptosis. Ezrin gene targeting by RNAi can inhibit the metastatic growth and migration of SGC-7901 human gastric cancer cells.

Suppression of Akt1 expression by small interference RNA inhibits SGC7901 cell growth in vitro and in vivo

The Akt/PKB kinase family, including Akt1, 2 and 3, plays critical roles in regulating cell growth, proliferation, survival, metabolic and many other cellular activities. Recent evidence indicates that PKB/Akt is frequently constitutively active in many types of human cancer including gastric cancer. In the present study, we applied immunohistochemistry to tissue microarray to detect the expression of Akt1, followed by Akt1 small interference RNA (siRNA) to examine knock down of the Akt1 gene on the growth inhibition of human gastric cancer SGC7901 cells. Our results indicate that the expression of Akt1 was significantly increased in gastric cancer compared to normal gastric tissue and adjacent non-cancer tissue. The in vitro study shows that cell growth was significantly inhibited and G0/G1 arrest was observed in siRNA-Akt1-treated group. In vivo, the size of tumors was significantly smaller in SGC7901 subcutaneous mice model treated with siRNA-Akt1 than those treated with siRNA-nonsense and PBS. Our studies demonstrated siRNA-Akt1 can inhibit Akt1 expression, exerted growth inhibition effect on SGC7901 cells in vitro and in vivo. Suppression of Akt1 expression by siRNA could be a new strategy in gastric cancer treatment.