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Objective To investigate the effect of different gene expression levels of Syntenin on invasion and mi?gration of glioma cells and the underlying molecular mechanisms. Methods Lentiviral RNA interference was used to knockdown the expression of syntenin in U-87 cells. Real-time quantitative PCR was used to detect mRNA expression levels of syntenin . Transwell assay and adhesion assay were used to examine the invasion, migration and adhesion, re?spectively. Western-blot was used to detect the protein expression levels of Syntenin, AKT, p-AKT, and MMP-9. Re?sults The mRNA expression level of Syntenin was greatly reduced in interference group compared with empty vector group (P0.05). Conclusion Syntenin may enhance the invasion and migration ability of glioma though up-regulation of p-AKT, which in turn pro?motes MMP-9 expression in a corresponding signal transduction pathway.
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AIM:To investigate the effects of fucoidan on the angiogenesis of multiple myeloma cells in vitro, and its related mechanisms .METHODS:The human multiple myeloma RPMI 8226 cells and human endothelial cells were cultured in vitro.The growth inhibition rate of RPMI 8226 cells was examined by MTT assay .The cell cycle and apoptosis rate were measured by flow cytometry .RPMI 8226 cells were treated with fucoidan for 72 h, and the cell culture superna-tant was collected .The VEGF concentration was examined by ELISA , and the tube formation assay was applied to assess the angiogenic activity .After treatment with fucoidan for 72 h at different concentrations , the protein levels of HIF-1α, VEGF, p-AKT and p-ERK1/2 were detected by Western blot .RESULTS: Fucoidan inhibited the growth of RPMI 8226 cells in a dose-and time-dependent manner .After treatment with fucoidan for 72 h, the cell cycle was arrested at G 1 phase , and the apoptotic rate of RPMI 8226 cells was increased with the increasing concentration of fucoidan , which was much higher than that in control group (P<0.05).The VEGF concentration was significantly decreased with the increa-sing concentration of fucoidan .The numbers and areas of the capillary-like structures decreased while the concentration of fucoidan increased, and those at 100 mg/L were less than those in the control (P<0.05).The protein levels of HIF-1α, VEGF, p-AKT and p-ERK1/2 in fucoidan group were significantly lower than those in control group (P<0.05).CON-CLUSION:Fucoidan inhibits the secretion of VEGF in multiple myeloma cells , and reduces angiogenesis induced by mul-tiple myeloma cells .It inhibits the protein expression of HIF-1αand VEGF , which may be related to inhibiting the phos-phorylation of AKT and ERK1/2.
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Objective:To explore the effect of calcium release-activated calcium channel modulator 1 (ORAI1) on the migration and invasion of colon cancer cell line SW480 and its mechanism. Methods:The SW480 cells were infected with ORAI interference lentivirus. The expression of ORAI1 mRNA and protein was confirmed by quantitative real-time polymerase chain reaction and Western blot. Transwell chamber, adhesion, angiogenesis, and vasculogenic mimicry experiments were conducted to detect the ability of cell invasion, migration, and angiogenesis and the intercellular adhesion of homogeneous and heterogeneous cells among each group. Confocal microscopy was employed to detect the difference of store-operated Ca2+entry (SOCE) in each group. Western blott was used to detect the expression of ERK1/2, p-ERK1/2, MMP-2, VEGF, and E-cadherin protein. Results:After the infection of SW480 with the ORAI1 interference lentivirus for 72 h, significant fluorescence expression was observed. Compared with the empty vector group and control group, the expression of ORAI1 was lower in the interference group (P<0.01). Invasion and migration ability decreased (P<0.01); the intercellular adhesion ability of homogeneous cells increased (P<0.05); the intercellular adhesion ability of heterogeneous cells decreased (P<0.05);the angiogenesi and vasculogenic mimicry were enhanced (P<0.01);the internal flow peak of SOCE was low (P<0.05); the expression of p-ERK1/2, MMP-2, and VEGF proteins decreased (P<0.01); and the expression of E-cadherin protein increased (P<0.01). Conclusion:ORAI1 may promote the migration and invasion of SW480. This mechanism may be associated with the increase of SOCE.
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<p><b>OBJECTIVE</b>To investigate the effect of 1,25-dihydroxyvitamin D(3) and 5-fluorouracil, either alone or in combination, on the expression of IGFBP-3 in human esophageal carcinoma 109 cell xenograft in nude mice.</p><p><b>METHODS</b>In vitro cultured esophageal carcinoma Eca-109 cells were inoculated subcutaneously in BALB/c mice. The tumor-bearing mice were randomly divided into control group (A), 1,25-dihydroxyvitamin D(3) group (B), 5-fluorouracil group (C), and 1,25-dihydroxyvitamin D(3) plus 5-fluorouracil group (D). 1,25-dihydroxyvitamin D(3) and 5-fluorouracil were administered at the doses of 2.5 ug/kg and 25 mg/kg via intraperitoneal injections, respectively, and the mice in the control group received saline injection only. The tumor growth was observed and the expression of IGFBP-3 in the tumor xenograft was detected using immunohistochemistry. An automatic biochemistry analyzer was used to determine serum calcium levels, and Von Kossa staining was utilized for observation of calcium deposition in the kidneys.</p><p><b>RESULTS</b>Compared with that in group A, the xenograft in groups B, C, and D all showed a lowered growth rate with a smaller tumor volume, and presented with stronger IGFBP-3 positivity and significantly higher levels of IGFBP-3 protein expression (P<0.05). In group D, the protein expression of IGFBP-3 was significantly increased compared with that in groups B and C (P<0.05). Compared with that in group A, serum calcium level was slightly increased in groups B, C, and D, , but no obvious calcium deposition was found in the kidney tissue sections.</p><p><b>CONCLUSION</b>Both 1,25-dihydroxyvitamin D(3) and 5-fluorouracil can inhibit the growth of the tumor xenograft in nude mice, and their combination is more effective. This effect is probably associated with increased protein expression of IGFBP-3 in the xenograft tumor. No calcium deposition occurs in the kidney tissue of the tumor-bearing mice.</p>
Subject(s)
Animals , Humans , Male , Mice , Cell Line, Tumor , Fluorouracil , Pharmacology , Insulin-Like Growth Factor Binding Protein 3 , Metabolism , Mice, Inbred BALB C , Mice, Nude , Vitamin D , Pharmacology , Xenograft Model Antitumor AssaysABSTRACT
Objective:To isolate breast cancer stem/progenitor cells from human breast cancer and study their proliferation and differentiation biological characteristics over long-term passages in vitro. Methods:Human breast cancer stem/progenitor cells were enriched in suspension cultures as nonadherent mammospheres(MS). Serial sphere formation assay was performed to determine self-renewal ability of mammosphere-derived cells (MSDC). Differentiation was induced by culturing MSDC in DMEM-F12 supplemented with serum but without growth factors. The ratio of CD44~+/CD24~(-/low) cell population was evaluated by flow cytometry(FCM). Results:The mammospheres were formed after inoculation of primary breast cancer cells into culcutre medium with growth factors but without serum. The mammospheres contained undifferentiated cells similar to stem cells, which had self-renewal and extensive proliferation capabilities. With increasing passages, the cells tended to adhere and differentiate. The number of adhering and differentiating cells increased, and the amount and size of mammospheres decreased. The CD44~+/CD24~(-/low) cell population was enriched in the basal-like molecular subtype of human breast tumors. The biological behaviors of mammospheres varied between different specimens.Conclusion:Cancer cells with stem cell properties of self-renewal, indefinite proliferation and multi-lineage differentiation widely existed in human breast cancer tissues. The biological behaviors varied because of different origin of specimens and changed under the effects of environmental factors.
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Objective To investigate the effect of integrin β4 expression on the metastasis potential of human thyroid follicular cancer cells. Methods Metastasis potential was observed and grouped in human thyroid follicular cancer cell line, CGTHW-1 cells, depending on the cells' penetrating ability in artificial matrigel. The expression of integrin β4 mRNA and protein were determined by immunocytochemistry, Western blot, and semiquantitative RT-PCR. Results The mRNA and protein expressions of integrin β4 were significantly higher in cells with high metastasis potential [0.277 5 ±0.034 0 vs 0. 187 5 ±0.022 2 ( Immunohistochemistry ), 0. 099 7 ± 0.0185 vs 0.039 0±0.010 2(Western blot), 0.555 0±0. 101 2 vs 0.270 0±0.029 9(RT-PCR), all P＜0.01]. Conclusion Integrin β4 may play an important role in human thyroid cancer invasion. It seems probably to be a potential target for human thyroid cancer treatment.
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<p><b>OBJECTIVE</b>The objective of this paper was to study the change of P38MAPK and Fas in the apoptosis of THP-1 cells induced by allicin.</p><p><b>METHOD</b>The proliferation inhibition rates of THP-1 cells after various treatments were examined by MTT assay. Apoptosis rate was determined with Annexin V- FITC/PI double staining by flow cytometry. The expression and distribution change of the phosphorylation p38MAPK (P-p38MAPK) were detected by immunohistochemical staining. The changes of P-p38 MAPK and Fas proteins were detected by Western blot.</p><p><b>RESULT</b>The proliferations of leukemia cell line THP-1 are inhibited by allicin. MTT assay showed that allicin can inhibit the proliferation of the THP-1 cell, and the inhibition was dependent on both dose and time. The IC50 of 72 hours was 12.8 mg x L(-1). Apoptosis rate detected by Annexin V-FITC/PI was proportional to the concentration of the allicin. After the immunohistochemical staining test, the P-p38MAPK was located in the cell nucleus and plasma, showing deep brown, when adding allicin to THP-1 cell. Western blot test showed that the P-p38MAPK proteins expression was proportional to the concentration of Allicin and was also dose dependent. The levels of P-p38MAPK in negative control group, 1/2 IC50 of 72 hours group and IC50 of 72 hours group were 0.259 8 +/- 0.013 2, 0.61 2 +/- 0.008 3 and 0.505 6 +/- 0.005 5 respectively, and the levels of Fas proteins were 0.287 4 +/- 0.008 9, 0.426 8 +/- 0.007 9 and 0.597 1 +/- 0.010 9 respectively. The difference was statistically significant when compared with the negative control group (P < 0.01).</p><p><b>CONCLUSION</b>Allicin can significantly induce THP-1 cells apoptosis, and its mechanism may be related to the activation of P38MAPK/Fas.</p>
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Humans , Apoptosis , Cell Line, Tumor , Neoplasms , Drug Therapy , Metabolism , Phosphorylation , Signal Transduction , Sulfinic Acids , Pharmacology , p38 Mitogen-Activated Protein Kinases , Genetics , MetabolismABSTRACT
Objective To investigate the expression of platelet-derived growth factor-D (PDGF-D) and bascular endothelial growth factor(VEGF) in gastric carcinoma and elucidate the potential relationship between their overex-pression and clinical pathological characteristics. Methods Immunohistochemical assay was performed to detect the protein expression of PDGF-D and VEGF in tissues. Semiquantitative reverse transcription polymerase chain re-action (RT-PCR) was performed to evaluate the mRNA expression of PDGF-D and VEGF in part of random selec-ting gastric carcinoma samples. The correlation between the expression of PDGF-D and VEGF, and the relationship between the expression of PDGF-D, VEGF and the clinical pathological characteristics were analyzed. Results The protein expression of PDGF-D and VEGF in gastric carcinoma tissues were significantly higher than that in adjacent tissues and normal gastric mucosa(P <0.05) ;The expression of PDGF-D and VEGF correlated with TNM staging, depth of invasion and lymphatic metastasis (P < 0.05), while the expression of PDGF-D also correlated to histolog-ical differentiation (P < 0.05). There was a significant positive correlation between PDGF-D and VEGF at the mR-NA and protein expression levels (P < 0.05). Conclusion PDGF-D and VEGF specifically highly expressed in gastric carcinoma. The abnormal expression may play an important role in the carcinogenesis and metastasis of gas-tric carcinoma.
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Objective To investigate the expression of platelet-derived growth factor-D(PDGF-D) and bascular endothelial growth factor(VEGF) in gastric carcinoma and elucidate the potential relationship between their overexpression and clinical pathological characteristics.Methods Immunohistochemical assay was performed to detect the protein expression of PDGF-D and VEGF in tissues.Semiquantitative reverse transcription polymerase chain reaction(RT-PCR) was performed to evaluate the mRNA expression of PDGF-D and VEGF in part of random selecting gastric carcinoma samples.The correlation between the expression of PDGF-D and VEGF,and the relationship between the expression of PDGF-D,VEGF and the clinical pathological characteristics were analyzed.Results The protein expression of PDGF-D and VEGF in gastric carcinoma tissues were significantly higher than that in adjacent tissues and normal gastric mucosa(P
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<p><b>BACKGROUND</b>To investigate the ability of alveolar macrophage (AM) and peripheral blood monocyte (PBMC) from lung cancer patients to produce Interleukin-10 (IL-10) and to evaluate the local and general cellular immune state of lung cancer patients.</p><p><b>METHODS</b>AM and PBMC were obtained from 57 patients with lung cancer, 33 patients with benign pulmonary diseases and 12 healthy volunteers. IL-10 in the culture supernatants was measured quantitatively by ELISA.</p><p><b>RESULTS</b>(1) Elevated levels of IL-10 produced by PBMC were found in lung cancer group with respect to healthy volunteers and patients with benign pulmonary diseases (148.60±35.56 vs 93.83±9.22 and 108.91±15.95 ng×L⁻¹ respectively) (P < 0.001). The level of IL-10 by AM from lung cancer patients was 132.06±30.42 ng×L⁻¹, which was remarkably higher than that of healthy volunteers (92.67±11.22 ng×L⁻¹) and benign pulmonary diseases (94.39±10.04 ng×L⁻¹) (P < 0.001). (2) The level of IL-10 produced by PBMC from lung cancer group of stage IV was significantly higher than that of stage I+II (178.33±13.52 vs 131.57±25.35 ng×L⁻¹) (P < 0.001). AM from lung cancer patients of stage III and IV produced more IL-10 than that of stage I+II did (150.13±15.57 and 160.50± 18.75 vs 117.05±28.12 ng×L⁻¹ respectively) (P < 0.001); PBMC from small cell lung cancer patients produced higher level of IL-10 than squamous cell carcinoma and adenocarcinoma did (194.83±23.88 vs 140.37± 27.00 ng×L⁻¹ and 136.50±27.39 ng×L⁻¹ respectively) (P < 0.01). AM from small cell lung cancer patients produced higher levels of IL-10 than squamous cell carcinoma and adenocarcinoma did (165.33±23.78 vs 127.74±26.19 ng×L⁻¹ and 120.30±29.66 ng×L⁻¹ respectively) (P < 0.01); Size of mass and performance status greatly affected the level of IL-10; IL-10 level of lung cancer patients with survival time more than 2 years was remarkably lower than that of patients with survival time less than 2 years (P < 0.01).</p><p><b>CONCLUSIONS</b>Higher level of IL-10 presents both in local and general body of lung cancer patients. IL-10 may play an important role in deterioration of lung cancer. Detection of IL-10 level may be helpful to evaluate cellular immunity and predict prognosis of lung cancer patients.</p>
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Objective To investigate the effects of curcumin on the proliferation, cell cycle distribution, and apoptosis of the acute myeloid leukemic cell line HL 60 and the hepatocarcinoma cell line QGY. Methods MTT method was used to detect the biological activities of curcumin at different concentrations and at different time. The cell cycle distribution was analyzed by flow cytometry, and changes of the cellular ultrastructure were observed by electronic microscopy. Results Curcumin could inhabit the growth of HL 60 and QGY in dose and time dependent manners. IC50 values of curcumin at 72 h to HL 60 and QGY were 24.8 ?mol/L and 49.5 ?mol/L, respectively. The cell growth of HL 60 was arrested at S and G 2/M stages (apoptosis peak: 8.65%), and that of QGY was arrested at S stage (apoptosis peak: 10.84%). Curcumin could lead to fat degeneration in HL 60 cells and cell degeneration and necrosis of QGY cells, resulting in apoptosis of QGY cells. Conclusion Curcumin has inhibitory effect on the growth of HL 60 cells through its anti proliferation and on QGY cells through the induction of apoptosis of QGY cells.
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Aim To study the effect of tubeimosides on human rectal cancer cell line SW480 in vitro and the mechanisms of its antitumor effect.Method The morphological changes were determined by means of light microscopy and electron microscopy respectively.Cell apoptosis was detected by flow cytometry through Annexin V assay and PI fluorescent staining methods.The protein levels of Bc1-2,p53 and Fas were determined using immunohistochemical technique.Results Apparent morphological characteristic of apoptosis was detected under the optical and electric microscope.The percentage of apoptotic cell increased when comparing the drug groups with control after treatment with tubeimoside Ⅰand Ⅲ.Immunohistochemical analysis revealed apoptosis was and induced by tubeimosides through inhibiting Bcl-2 and p53,and upregulating Fas.Conclusion Tubeimosides can induce apoptosis of SW480 cells,which may be one reasons of its antitumor effects.
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Objective To investigated the effect of somatostatin(SS)on cholecystokinin-induced alterations of exocrine function and the redistribution of the F-actin in the pancreatic acinar cells.MethodsIn vitro,isolated rat pancreatic acini were divided into 12 groups:normal control group,different concentrations ofcholecystokinin-octapeptide groups(CCK-8)of 10-12,10-11,10-10,10-9 or 10-8 mol/L,SS group(10-7mol/L),SS and different dose CCK-8 groups.The acinar cells were stimulated with different concentrations of CCK-8 for 30 min in the presence or absence of 10-7 mol/L SS.Amylase and trypsin activity were measured using corresponding assay kits,and F-actin distribution in pancreatic acinar cells were detected by laser confocal microscopy.ResultsSS stabilized the structure of cytoskeleton in acinar cells,and remarkably increased the ratio of subapical/basolateral F-actin(P
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Objective To construct an siRNA expression plasmid against tumor susceptibility gene 101(tsg101) and investigate its effect of RNA interference on oxaliplatin(L-OHP)-resistant human colon cancer cell line HT29/L-OHP.Methods The targeting fragments specifically against tsg101 were designed according to the principle of small interfering RNA designation using an online software.The sequences were cloned into siRNA expression plasmids,and the plasmids were transfected into HT29/L-OHP cells.The expression of tsg101 mRNA after the transfection of TSG101-siRNA plasmid was detected by RT-PCR.The expression of TSG101 after TSG101-siRNA transfection was detected by Western blotting.MTT test was applied to measure the inhibition combined with L-OHP on the proliferation of HT29/L-OHP cells.Distribution of cell cycle was analyzed using flow cytometry after RNA interference to HT29/L-OHP cells.Results The expected fragments were designed,and the TSG101-siRNA plasmid was confirmed by DNA sequencing.The TSG101-siRNA plasmid inhibited the expression of tsg101 mRNA,and the expression of TSG101 protein,and suppressed the proliferation of HT29/L-OHP cells obviously when combined with oxaliplatin.The analysis of cell cycle indicated that the TSG101-siRNA plasmid reduced the cells in G2/M phases and increased the cells in G0/G1 and S phases.Conclusion The expression vector of TSG101-siRNA combined with oxaliplatin inhibits the proliferation of HT29/L-OHP cells and increases the sensitivity to chemotherapy.
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Objective To investigate the validity of selecting subclones of human breast cancer cells with high-and low-metastatic potentiality,based on their different ability of penetrating the matrigel in vitro,and analyze their biological characteristics.Methods Continuous in vitro invasion assays in matrigel were applied to screen two subclones of human breast cancer cell line MDA-MB-435s,characterized by high-and low-metastatic potentiality.Cell growth curve assay,invasion assay,adhesion assay and angiopoiesis-promoting assay were conducted to explore the different biological properties of these two subclone cells.Results Two subclones of MDA-MB-435s,of high-and low-metastatic potentiality respectively,were obtained through continuous in vitro invasion assay,manifesting significant difference in growth rate,invasion ability,adhesion ability and angiopoiesis-promoting ability.Conclusion It is feasible to obtain subclones of human breast cancer cells of high-and low-metastatic potentiality by utilizing their difference in penetrating the matrigel in vitro.
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Objective To establish a drug-resistant human colon cancer cell line to oxaliplatin(L-OHP)based on cell line HT29.Methods A resistant cell line-HT29/L-OHP was established by gradually increasing the dose of L-OHP and intermittent administration.The growth curves,multidrug resistance and resistance index of HT29/L-OHP cell line to anticancer agents were detected by MTT assay.The changes of its biological characteristics were determined by light microscopy,electron microscopy,and flow cytometry.Results HT29/L-OHP cell line was established after 3 months,which had stable resistance to L-OHP and a resistance index of 10.64.HT29/L-OHP cells exhibited cross resistance to many other chemotherapeutic agents.As compared with parental cells,the morphological and chromatosome number of HT29/L-OHP were changed;its doubling time was prolonged;and the number of cells in S phase and G0/G1 phase were decreased while in G2/M phase increased.Conclusion HT29/L-OHP cell line shows the typical multidrug-resistant phenotype.
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Objective To observe the effects of oxaliplatin on proliferation in human colon carcinoma cell lines HT29 in vitro and investigate the mechanism. Methods The inhibition of proliferation in HT29 cell was estimated by MTT test. Morphologic changes were observed under electron microscope. Distribution of cell cycle and apoptosis was analyzed by using flow cytometry. The expression of cell cycle protein and apoptosis-associated gene protein was detected with immunohistochemical technique. Results Oxaliplatin could inhibit the proliferation of HT29 cells and the inhibition depended on the exposure dose and time. When treated with oxaliplatin for 72 h, apoptotic cells and apoptotic body could be found under the transmission electronic microscope. The analysis of cell cycle indicated that oxaliplatin blocked cells at G2/M phases and cells of G0/G1 and S phase reduced. The expression of Fas and Bax was up-regulated; Bcl-2, CyclinB1, and PCNA down-regulated. Conclusion Oxaliplatin could inhibit proliferation of the colon carcinoma cell lines HT29. The mechanism of inhibited proliferation is related to the induced apoptosis and the blocked cells.
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<p><b>OBJECTIVE</b>To investigate the effect of curcumin on the proliferation, cell cycle distribution and apoptosis of hepatocarcinoma cell line QGY.</p><p><b>METHODS</b>The MTT method was used to assay the biologic activities of curcumin in different times and different doses. The cell cycle distribution was detected by flow cytometic analysis. The cell ultrastructure was observed by electronic microscopy.</p><p><b>RESULTS</b>Curcumin could inhibit effectively QGY in a dose- and time- dependent manner. IC(50) of curcumin to QGY was 49.50 micromol/L in 72 hours. The cell growth was arrested at S stage. Curcumin could lead to the degeneration, necrosis, and apoptosis.</p><p><b>CONCLUSIONS</b>Curcumin can interrupt the cell cycle and has a role in cytotoxicity, antiproliferation and inducing apoptosis of QGY.</p>
Subject(s)
Humans , Antineoplastic Agents , Pharmacology , Apoptosis , Cell Cycle , Cell Division , Curcumin , Pharmacology , Dose-Response Relationship, Drug , Flow Cytometry , Liver Neoplasms , Drug Therapy , Pathology , Microscopy, Electron , Time Factors , Tumor Cells, CulturedABSTRACT
Objective To investigate the effect of phosphatidylinositol 3-kinase(PI3K) inhibitor wortmannin on migration and invasion of human thyroid follicular carcinoma cell line CGTHW-1 and its mechanism.Methods MTT colorimetric assay was used to select the optimal concentration and time of giving wortmannin.CGTHW-1 cells used in present study were divided into control group and experimental group(cultured in the medium with or without blood serum).Cells of experimental group were treated with wortmannin,and that of control group were given no treatment.The migration and invasion ability of CGTHW-1 cells was detected by scratch test and Transwell chamber assay respectively.Microfilament fluorescence staining with fluorescein isothiocyanate(FITC)-labeled phalloidin was performed to observe the morphologic changes in CGTHW-1 cells.The expressions of Rac1 protein and mRNA in CGTHW-1 cells were examined by immunocytochemistry staining and semiquantitative RT-PCR.Results When CGTHW-1 cells were cultured in serum medium,the migrating speed of the cells slowed down,and the number of cells passing through the Transwell chamber reduced significantly after being treated with wortmannin in experimental group(13.8?3.03) than in control group(41.6?6.95,P0.05).Conclusions Wortmannin can effectively depress the migration and invasion of human thyroid follicular carcinoma cells,and the depression effect may be due to cytoskeleton rearrangement induced by inhibiting the expression of Rac1(the downstream molecule of PI3K).PI3K and Rac1 are probably potential targets for human thyroid cancer treatment,which may provide a theoretical evidence for the drug treatment of thyroid cancer.
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Objective To investigate the antitumor mechanism of sodium arsenite on human gastric carcinoma cell line SGC-7901 in vitro. Methods MTT assay, light microscopy, electron microscopy, flow cytometry, and immunocytochemical staining were used to analyze the effect of sodium arsenite on biologic behavior of SGC-7901 cells. Results Sodium arsenite (2.50 ～ 40.00 ?mol/L) could inhibit the growth of gastric carcinoma cells, it depended on the duxation and concentration, and its 50% inhibitory concentration(IC50) was 8.69 ?mol/L after 72 hours' treatment. SGC-7901 cells were arrested significantly in G2/M phase treated with sodium arsenite for 48 and 72 hours. SGC-7901 cells presented typical morphologic feature of apoptosis and necrosis after exposure to sodium arsenite. Sodium arsenite up-regulated Caspase-3 protein expression in SGC-7901. Conclusion Sodium arsenite could obviously inhibit the proliferation of SGC-7901 cells, induce cell cycle arrest and apoptosis and necrosis of the cells. its mechanism is possibly associated with inhibition of elimination of ROS and the up-regulated expression of Caspase-3 protein.