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BACKGROUND: Immunotherapy enhances the anti-cancer immune response in many ways, so combined immunotherapy is a better choice. Ultrasoundtargeted microbubble destruction technique delivers drugs, genes, antibodies and cytokines directly to the cytoplasm of immune cells and enhances the immune response. However, the application of ultrasound-targeted microbubble destruction technique in the treatment of ovarian cancer with both CXC chemokine receptor 4 antibody and programmed death-ligand 1 antibody has not been reported. OBJECTIVE: To investigate the effect of ultrasound irradiation on the proliferation and migration of ovarian cancer cells with CXC chemokine receptor 4 antibody and programmed death-ligand 1 antibody double targeted nanobubbles. METHODS: IOSE-80 normal ovarian epithelial cells, SKOV3 and CAOV3 ovarian cancer cells were cultured and expanded. Double labeling fluorescence immunoassay was used to co-locate CXC chemokine receptor 4 and programmed death-ligand 1 protein. Western blot assay was used to detect the relative expression of CXC chemokine receptor 4 and programmed death-ligand 1 protein in three kinds of cells and screen out the experimental cells, i.e., pure nanobubbles, nanobubbles carrying CXC chemokine receptor 4 antibody, nanobubbles carrying CXC chemokine receptor 4 and programmed death-ligand 1 antibody. SKOV3 ovarian cancer cells in the logarithmic growth phase were taken and divided into six groups for treatment. Group A was added with McCoy's 5A medium. Group B was added with McCoy's 5A medium containing stromal cell-derived factor-1. Group C was added with pure nanobubble solution and McCoy's 5A medium containing stromal cell-derived factor-1. Group D was added with nanobubble solution containing CXC chemokine receptor 4 antibody and McCoy's 5A medium containing stromal cell-derived factor-1. Group E was added with nanobubble solution containing CXC chemokine receptor 4 and programmed death-ligand 1 antibody and McCoy's 5A medium containing stromal cell-derived factor-1. Pure nanobubble solution was added in group F. After ultrasonic irradiation for 120 seconds and incubation for 48 hours, the survival rate of cells was measured by CCK-8 assay, and the healing and migration ability of cells in groups B-E were measured by wound healing test. RESULTS AND CONCLUSION: (1) Immunofluorescence staining showed that CXC chemokine receptor 4 and programmed death-ligand 1 protein could be expressed in all three kinds of cells. Western blot assay showed that the expression levels of CXC chemokine receptor 4 and programmed death-ligand 1 in SKOV3 and CAOV3 ovarian cancer cells were significantly higher than those in IOSE-80 normal ovarian epithelial cells (P < 0.05). (2) CCK-8 assay results exhibited that the cell survival rate of group B was higher than that of group A (P < 0.05). The cell survival rate of group F was lower than that of group A (P < 0.05). The cell survival rate of groups B-E decreased gradually, and there were significant differences between the two groups (P < 0.05). (3) Wound healing test demonstrated that the cell healing rate of groups B-E decreased gradually, and there were significant differences between the two groups (P < 0.05). (4) The results show that the use of CXC chemokine receptor 4 antibody and programmed death-ligand 1 antibody double targeted nanobubbles under ultrasoundtargeted microbubble destruction can significantly inhibit the proliferation and migration of ovarian cancer cells. [ABSTRACT FROM AUTHOR]

Background and purpose: Gastric cancer is one of the common gastrointestinal malignancies. FKBP1A has been reported to be involved in the occurrence and development of various tumors, but the biological role and mechanism of it in gastric cancer remain unclear. This study aimed to investigate the expression level and prognostic value of FKBP1A in gastric cancer tissues, and to analyze the possible pathways and mechanisms of its regulation of gastric cancer progression. Methods: The expression of FKBP1A in gastric cancer was observed by immunohistochemistry, and its correlation with poor prognosis was analyzed by combining bioinformatics and clinicopathological parameters. Kaplan-Meier survival curve was used to analyze the effect of FKBP1A on the 5-year survival rate of patients with gastric cancer after surgery, and COX multivariate regression analysis was used to explore the independent prognostic factors affecting the 5-year survival rate of patients with gastric cancer after surgery. The diagnostic value of FKBP1A expression in patients with gastric cancer was analyzed using receiver operating characteristic (ROC) curve. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) were used to enrich and analyze the biological function of FKBP1A and the possible signal pathways involved. We constructed the MGC803 cell model transfected with lentivirus in vitro, explored the influence of FKBP1A on the glucose metabolism and malignant biological behavior of MGC803 cells, and the possible molecular mechanism involved, and established a nude mouse transplantation tumor model in vitro to verify it. Results: Immunohistochemical results showed that FKBP1A was highly expressed in gastric cancer (P＜0.01), and bioinformatics and clinical parameter analysis showed that FKBP1A was associated with poor prognosis. Kaplan-Meier survival analysis and COX regression analysis showed that the expression level of FKBP1A was negatively correlated with 5-year survival. And carcinoembryonic antigen (CEA)≥5 μg/L, carbohydrate antigen (CA) 19-9≥37 kU/L, T stage (T3-T4) and N stage (N2-N3) were independent prognostic factors affecting the 5-year survival rate of gastric cancer patients after surgery (P＜0.05). ROC analysis showed that high expression of FKBP1A had good prognostic value (P<0.01). Enrichment of GO and KEGG suggested that FKBP1A was involved in regulating glucose metabolism in gastric cancer cells. In vitro experiments showed that overexpression of FKBP1A promoted glucose metabolism and proliferation, invasion and migration of MGC803 cells, while silencing of FKBP1A did the opposite (P＜0.05). In vivo experiments showed that overexpression of FKBP1A in gastric cancer cells promoted the growth of transplanted tumor in nude mice, while silencing FKBP1A inhibited it (P＜0.05). Mechanism analysis showed that overexpression of FKBP1A upregulated the expressions of phosphatidylinositol 3-kinase (PI3K) and protein kinase B (AKT) in gastric cancer cells, while silencing FKBP1A downregulated the expressions (P＜0.05). Conclusion: FKBP1A is highly expressed in gastric cancer tissues, and is associated with poor prognosis, which may be due to the promotion of glucose metabolism and malignant biological behavior of gastric cancer cells by activating PI3K/AKT. [ABSTRACT FROM AUTHOR]

Objective: To investigate the therapeutic effect and possible mechanism of sinomenine(SIN) on type 2 diabetic(T2DM) mice with liver cancer(HCC). Methods: Eight-week-old male BALB/c mice(20-25 g) were divided into Control, T2DM+HCC,SIN-L, SIN-M and SIN-H group. Mice in the Control group were fed normally, and mice in other groups were injected intraperitoneally with streptozotocin(STZ) and inoculated with hepatocellular carcinoma cells(H22) in liver parenchyma to establish T2DM combined with HCC mice model. Mice in the SIN-L, SIN-M and SIN-H group were intraperitoneally injected with 10, 20 and 40 mg/kg/d of sinomenine, respectively. Mice in the Control group and T2DM+HCC group were intraperitoneally injected with 0.5 m L of normal saline respectively. All the mice were treated for 21 days. 24 hours after the last administration, the liver index was calculated and fasting blood glucose(FPG), fasting insulin(FINS), serum total cholesterol(TC), triglyceride(TG)], alanine aminotransferase(ALT), aspartate aminotransferase(AST) and lactate dehydrogenase(LDH), liver superoxide dismutase(SOD), catalase(CAT), Glutathione peroxidase(GSH-PX)and malondialdehyde(MDA) levels were detected. Liver morphology was observed by hematoxylin and eosin(HE) staining. The protein expression of BCL2, BAX, P53, signal transducer and activator of transcription 3(STAT3), cytokine signal inhibitor 3(SOCS3) and sterol regulatory element binding protein-1(SREBP-1) in liver tissue were detected by Western blot. Results: The median survival time of T2DM+HCC group, SIN-L group, SIN-M group and SIN-H group was 25, 32, 35 and 41 days respectively(P＜0.001), the median survival time of mice extended with the increase of sinomenine concentration. Compared with T2DM+HCC group, the levels of FPG, FINS, TC and TG in SIN-L, SIN-M and SIN-H group decreased, serum ALT, AST and LDH levels decreased, the basic rules of hepatic cell arrangement, edema, vacuolar degeneration, inflammatory cell infiltration and other lesions were significantly reduced, liver index decreased, liver SOD, CAT and GSH-PX levels increased, liver MDA level decreased, liver BCL2 protein expression decreased, liver BAX and P53 protein expression increased(P＜0.05). Compared with T2DM+HCC group, the expression of p-STAT3(Tyr705), SOCS3 and SREBP-1 protein in liver of SIN-L, SIN-M and SIN-H group decreased in a dose-dependent manner(P＜0.05). Conclusion: Sinomenine can effectively prolong the survival time of type 2 diabetic mice with liver cancer, improve the blood glucose and lipid levels as well as the live function, and inhibit the growth of cancer cells, which may be related to the inhibition of STAT3 signaling pathway. [ABSTRACT FROM AUTHOR]

Breast cancer is the most common malignant tumor in women and the main cancer causing death in females. Breast cancer therefore seriously threatens women's health and life span. Although there are a variety of comprehensive and multidisciplinary treatments for different types of breast cancer, the overall prognosis of advanced breast cancer remains unsatisfactory. The incidence of breast cancer is increasing year by year, and the age of onset is gradually decreasing, making the discovery of a breakthrough in breast cancer treatment a major problem that needs to be solved urgently. A large number of studies have shown the growth of breast cancer cells can be inhibited by inducing ferroptosis. Acid sphingomyelinase has also been confirmed to be involved in cell death induced by ferroptotic agonists. This article reviews the progress in the use of acid sphingomyelinase and ferroptosis in the treatment of breast cancer, and summarizes the mechanism of ferroptosis in breast cancer cells and its correlation with acid sphingomyelinase. This review will provide a theoretical foundation for seeking new therapeutic targets for breast cancer. [ABSTRACT FROM AUTHOR]

Methods: The cancer genome atlas(TCGA. https://portal.gdc.cancer.gov/) database was used to analyze the dif- ferential expression of LncRNA FAR2P1. According to the follow-up data of 169 breast cancer patients with high expression of LncRNA FAR2P1 and 1180 breast cancer patients with low expression of LncRNA FAR2P1, the relation between LncRNA FAR2P1 and the prog- nosis was analyzed. Qrt-per was used to explore the expression of LncRNA FAR2P1 in McF-10a and MDA-MB-231 SKBR3 cells. The effects of FAR2P1 on the proliferation and migration of cells were evaluated by in vitro experiments, such as Cell Counting KIT-8 (CCK8) method. EDU method, clone formation method and Transwell method. Flow cytometry was used to detect whether FAR2P1 reg- ulates the apoptosis process of cells. The regulatory effect of FAR2P1 on cell proliferation in vivo was further investigated. Results: The expression of lncRNA FAR2P1 is obviously increased in breast cancer tissues and cell line MDA-MB-231 SKBR3, and is negatively relate with the prognosis of patients. Compared with the control, the silencing FAR2P1 significantly reduced the proliferation and migration ability of MDA-MB-231 and SKBR3, but improved the proportion of apoptosis. In vivo xenogenic tumor model showed that silencing FAR2P1 markedly decreased the proliferation ability of breast cancer compared with the control groups. Conclusion: LncRNA FAR2P1 is highly expressed in breast cancer and plays an important role in regulating the proliferation, apoptosis and migration of breast cancer. [ABSTRACT FROM AUTHOR]

Background and purpose: The novel centrosomal regulatory protein Sec23 homolog B (SEC23B) regulates autophagy in cells, thereby providing energy and nutrients that contribute to tumor growth and distant metastasis. However, whether this role is involved in the mechanism of infiltrative metastasis in breast cancer is unclear. The aim of this study was to investigate the molecular mechanism by which SEC23B promotes breast cancer infiltration and metastasis. Methods: The association between SEC23B expression and breast cancer prognosis and metastasis was analyzed using Kaplan-Meier Plotter database and HCMDB database. MCF-7 cells were divided into vector group (control) and SEC23B overexpression plasmid group (SEC23B), and MDA231-LM2 cells were divided into SEC23B knockdown group (sh-SEC23B) and control group (sh-NC). Western blot was used to detect the expressions of SEC23B, autophagy-associated proteins [dead bone fragment 1 (SQSTM1, p62), microtubule-associated-protein light-chain-3 (LC3)] and extracellular-regulated protein kinases (ERK)/mammalian target of rapamycin (mTOR) pathway proteins in breast cancer cells. Cell migration was assessed by transwell assay and wound healing assay, and autophagic granules in cells were detected by immunofluorescence staining. In addition, an in vivo intraperitoneal tumor model was constructed to study the effect of SEC23B on breast cancer cell metastasis in vivo. Results: The overall survival of breast cancer patients with high SEC23B expression was significantly shorter than that of patients with low SEC23B expression. The expression of SEC23B in metastatic breast cancer was significantly higher than that in breast cancer without metastasis. SEC23B protein levels were lower in primary breast cancer cells (MCF-7, BT-549, MDA-MB-468 and MDA-MB-453) than in metastatic breast cancer cells (MDA231- LM2 and ZR-75-30). Compared with the control group, the SEC23B group significantly accelerated cell migration (P<0.001). Compared with the sh-NC group, the sh-SEC23B group significantly reduced cell migration (P<0.001). Compared with the control group, the expression level of LC3A/B and the formation of autophagy particles in the SEC23B group were significantly increased, while the expression of p62 protein and the phosphorylation levels of mTOR and ERK were decreased. Compared with the sh-NC group, the LC3A/B expression level and the formation of autophagy particles were significantly decreased in the sh-SEC23B group, and the phosphorylation levels of mTOR and ERK were increased, especially under starvation conditions. In in vivo experiments, tumor weight was significantly lower in the sh-SEC23B group compared with the sh-NC group (P<0.01), and there was an increase in necrotic tissue and a decrease in tumor metastasis in lung tissue in mice. sh-SEC23B group mice had a significantly lower number of lung metastatic tumors and LC3 immunohistochemical staining than the sh-NC group (P<0.01). Conclusions: SEC23B induces breast cancer autophagy and promotes cancer cell metastasis by inhibiting ERK/mTOR signaling pathway. [ABSTRACT FROM AUTHOR]

Background and purpose: Breast cancer is the most common malignancy in women, and it is also the cancer with the highest number of new cases worldwide in 2020. Human epidermal growth factor receptor 2 (HER2)-positive breast cancer accounts for approximately 20% of all breast cancers, which indicates higher rate of recurrence and metastasis and a poor prognosis. Therefore, it is of great significance to explore the biomarkers related to HER2-positive breast cancer. This study aimed to investigate the expression of circ-0003910 in HER2-positive breast cancer tissues and cells, and to clarify the effect of circ-0003910 on the migration and invasion of breast cancer cells. Methods: Circular RNA (circRNA) microarray was used to screen circRNA differentially expressed in HER2-positive breast cancer cells, and significantly overexpressed circRNA was selected as the research target. Fluorescence in situ hybridization (FISH) assay was used to detect the subcellular localization of circ-0003910. BaseScope assay was used to analyze the expression and clinical significance of circ-0003910 in breast cancer tissues. Circ-0003910 overexpressed and knockdown breast cancer cells were constructed by transfection of cloned plasmid and siRNA in vitro. The effect of circ-0003910 on the migration and invasion ability of breast cancer cells was detected by transwell assay. The molecular mechanism of circ0003910 promoting the migration and invasion of breast cancer cells was preliminarily explored by TMT quantitative proteomics techniques. Results: CircRNA microarray analysis showed that a total of 1 843 differentially expressed circRNAs were screened in HER2-positive breast cancer cells (fold change≥2, P<0.05), including 845 upregulated circRNAs and 998 downregulated circRNAs. Compared with normal breast epithelial cells, the differential expression ratio of circ-0003910 in HER2-positive breast cancer cells was 24.39. Real-time fluorescence quantitative polymerase chain reaction (RTFQ-PCR) results showed that the expression of circ0003910 was higher in HER2-positive breast cancer cells than in other molecular types of breast cancer cells, and BaseScope assay verified that circ-0003910 was mainly located in the cytoplasm of HER2-positive breast cancer tissue cells. Overexpression of circ0003910 promoted the migration and invasion of breast cancer cells, while circ-0003910 knockdown produced the opposite effects. Proteomics identification showed that 197 proteins were changed after overexpression of circ-0003910, of which 104 proteins were upregulated and 93 proteins were downregulated. GO and KEGG enrichment analysis suggested that circ-0003910 may be involved in biological processes such as cell adhesion molecule synthesis, transcriptional dysregulation in cancer, and protein digestion and absorption. Conclusion: Circ-0003910 is upregulated in breast cancer cells and can promote the migration and invasion of breast cancer cells, which may be a new biomarker and target for the treatment of metastatic breast cancer. [ABSTRACT FROM AUTHOR]

Breast cancer is a malignant tumor with the highest incidence in women in the world, and it represents the leading cause of cancer-related deaths in women. Breast cancer is a highly heterogeneous disease, including the heterogeneity between tumors and even within the tumor microenvironment, making precise classification and treatment of the disease difficult. The application of traditional high-throughput sequencing technology in breast cancer research has provided an important reference for revealing the occurrence and development of breast cancer, driving genes, precise classification, diagnosis and treatment. However, the limitation of traditional high-throughput sequencing technology is its inability to explore heterogeneity within the tumor microenvironment. The single-cell sequencing technology emerged in recent years has been greatly improved in terms of sensitivity, accuracy and efficiency, enabling us to analyze single-cell genome information in complex mixed cells, which has shown great performance in studying tumor heterogeneity. In recent years, there are a number of important research results obtained by harnessing single-cell sequencing technology in breast cancer research, including analyzing breast cancer transcriptome at the single-cell level, exploring the heterogeneity of breast cancer microenvironment, breast cancer drug resistance mechanisms, the clonal heterogeneity and clonal evolution of breast cancer, and comprehensively mining single-cell public data resources to reveal the heterogeneity of breast cancer. This article reviewed important research in recent years regarding the application of single-cell sequencing technology in breast cancer era. We aimed to provide references for breast cancer researchers to manipulate the single-cell sequencing technology and promote the in-depth use of single-cell sequencing technology in breast cancer research. [ABSTRACT FROM AUTHOR]

To analyze the clinicopathological features and prognosis difference of Luminal B type breast cancer patients with different subtypes. The clinicopathological and follow-up data of 359 cases of primary Luminal B type breast cancer patients who were admitted to Xuhui And Lingang Hospitals of Shanghai Sixth People's Hospital from January 2006 to January 2016 were retrospectively analyzed. According to Luminal B type breast cancer molecular subtypes, the patients were divided into the human epidermal growth receptor 2 (Her-2) negative group (266 cases) and the Her-2 positive group (93 cases). The clinicopathological features difference of the two groups were compared. Kaplan-meier survival curve was drawn to analyze the difference of 5-year progression-free survival rate and overall survival rate between the two groups, and Cox proportional regression was used to analyze the influencing factors of the prognosis of Luminal B type breast cancer patients. TNM stage III～IV stage, tumor histological grade III grade, PR negative, Ki-67 high expression and lymph node metastasis proportion in Her-2 positive group were higher than those in Her-2 negative group (P＜ 0.05). The 5-year DFS and OS survival rates in Her-2 positive group were 12.90% and 40.86%, respectively, which were lower than 24.06% and 59.77% in Her-2 negative group (Log-Rank χ2 =14.500, 12.860, P=0.000, 0.000). TNM stage III～IV stage, lymph node metastasis, Her-2 positive and PR negativewere the risk factors for poor prognosis in Luminal B type breast cancer patients ( P ＜ 0.05). There are differences in TNM stage, tumor histological grade, lymph node metastasis, Ki-67 and PR expression in different molecular subtypes of Luminal B type breast cancer patients. Meanwhile, TNM stage, lymph node metastasis, Her-2 positive and PR negative are risk factors for poor prognosis in Luminal B type breast cancer patients. [ABSTRACT FROM AUTHOR]

Bone metastasis is one of the most serious complications in advanced breast cancer patients. Severe osteodynia, pathological fracture and other complications in bone metastasis of breast cancer can seriously affect the quality of life and shorten life span. In recent years, with the further understanding of the mechanism of bone metastases and the cross-talk between tumor cells and bone microenvironment, development and application of many new effective drugs have made significant progress in the treatment of bone metastasis of breast cancer. This article reviewed the mechanism of bone metastasis of breast cancer and current treatment advances. [ABSTRACT FROM AUTHOR]

Objective: To investigate the function of mutant KEAP1 and its mutation in lung cancer cells. Methods: Western blot were conducted to determine the expression of Nrf2 and its target gene HO-1 in lung cancer cells with or without KEAP1 mutation. A549-constantly expressing pMSCV, wild type KEAP1 and mutant KEAP1were established by retroviral transfection. The clonogenic assay was performed to explore the effect of wild type Keap1 and mutant Keap1 on the proliferation ability of lung cancer cells. Results: The protein expression of NRF2 downstream gene HO-1 in KEAP1 / NRF2 mutant lung cancer cell lines group were increased compared with the non-mutant lung cancer cell lines group, and the level of reactive oxygen species (ROS) in the mutant group was significantly inhibited compared with the control group (P<0.01). Wide-type KEAP1 overexpression decreased the mRNA and protein expression of NRF2 target genes, increased the MDA level and suppressed proliferation in A549 cells compared with empty vector-transfected A549 cells (P<0.01), while over expression of mutant KEAP1 caused no significant differences (P>0.05). Conclusions: KEAP1 mutation may cause the loss of KEAP1 function, KEAP1mutation may cause tumor genesis and development by changing the oxidative stress of tumor cells. [ABSTRACT FROM AUTHOR]

Objective: To study the differential expression of CELF6 in breast cancer and normal tissues and its prognostic significance in breast cancer. Methods: The expression of CELF6 in breast cancer tissues and normal breast tissues was analyzed by GEPIA. The clinical samples of breast cancer were used to study the expression level of CELF6 protein in breast cancer tissues compared with nomal tissues. KM-plotter was used to study the relationship between the expression of CELF6 and the prognosis survival of breast cancer patients. The effect of different CELF6 expression levels on the growth and proliferation of breast cancer cells was analyzed by CCK8 cell counting assay. Results: GEPIA online software analysis showed that CELF6 expression was significantly lower in breast cancer than in normal tissues (P<0.001). The results of immunohistochemistry showed that the positive expression of CELF6 in breast cancer tissues was significantly lower than that in normal tissues adjacent to cancer. The survival curve of KM-plotter online analysis showed that the survival prognosis of patients with high expression of CELF6 was significantly better than those with low expression (P<0.001). The CCK8 assay showed that the expression of CELF6 in the breast cancer cell line MDA-MB-231 was knocked down, the cell proliferation rate was significantly faster, and the proliferation rate of MDA-MB-231 cells overexpressing CELF6 was slowed down.Conclusions: CELF6 may be a potential tumor suppressor gene, which is lowly expressed in breast cancer tissues and is associated with poor prognosis in breast cancer patients. [ABSTRACT FROM AUTHOR]

Objective: To investigate the mechanism of the farnesoid X receptor (FXR) activation by GW4064 to inhibit the growth of colon cancer cells. Methods: The effects of specific FXR agonist (GW4064) on the growth of HT-29 cells were studied in vitro by MTT. The infiltration and metastasis of HT-29 cells were detected by the transwell inserts. The mRNA expression of FXR and MMP-7 were determined by RT-PCR, The protein expression of FXR and MMP-7 were measured byWestern blot. Results: MTT results showed that the growth inhibition rate of GW4064 in human colorectal HT-29 cells was concentration dependent; Transwell inserts results showed that GW4064 inhibited the invasion and metastasis of colon cancer cells. Compared with the control group, the difference was statistically significant (P<0.05). RT-PCR and Western blot display GW4064 promoted FXR mRNA and protein expression and inhibited the expression of MMP-7. The expression of mRNA and protein was significantly different from that of the control group (P<0.05). Conclusion: GW4064 inhibited metastasis of colon cancer cells. The expression of mRNA and protein of FXR was up-regulated by FXR specific agonist in cell line HT-29, and MMP-7 is just opposite. The activation of FXR may inhibit the metastasis of colon cancer cells by inhibiting MMP-7. [ABSTRACT FROM AUTHOR]

Objective To investigate the inhibiting effects of alcohol extract from Dioscore bulbifera on proliferation, colony formation and migration of cancer cell lines. Methods Alcohol extract from Dioscore bulbifera was prepared using Soxhlet extraction. Human gastric cancer cell line MGC803 was treated with different concentrations (0, 60, 120 mg/L) of alcohol extract from Dioscore bulbifera. In vitro, proliferation, colony formation and migration of gastric cancer cells were detected by MTT, colony formation experiments and Transwell assay respectively. Results The proliferation (day 2-day 6, F=29.130, 21.864, 67.826, 36.015, 43.656, P < 0.01)and colony formation (F=11.918, P < 0.01)of gastric cancer cells were significantly inhibited by administration of alcohol extract from Dioscore bulbifera at both 60 mg/L and 120 mg/L . The migration (F=4.258, P <0.05)of gastric cancer cells were significantly suppressed after cells were treated with 120 mg/L alcohol extract from Dioscore bulbifera. Conclusion Alcohol extract from Dioscore bulbifera significantly inhibit proliferation, colony formation and migration of gastric cancer cells. [ABSTRACT FROM AUTHOR]