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Toxicarioside A inhibits SGC-7901 proliferation,migration and invasion via NF-κB/bFGF signaling 被引量:8
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作者 Jun-Li Guo Shao-Jiang Zheng +10 位作者 Yue-Nan Li Wei Jie Xin-Bao Hao Tian-Fa Li Li-Ping xia Wen-Li Mei Feng-Ying Huang Yue-QiongKong Qi-Yi He, Kun Yang guang-hong tan Hao-Fu Dai 《World Journal of Gastroenterology》 SCIE CAS CSCD 2012年第14期1602-1609,共8页
AIM:To investigate the inhibitory role of toxicarioside A on the gastric cancer cell line human gastric cancer cell line(SGC-7901) and determine the underlying molecular mechanism.METHODS:After SGC-7901 cells were tre... AIM:To investigate the inhibitory role of toxicarioside A on the gastric cancer cell line human gastric cancer cell line(SGC-7901) and determine the underlying molecular mechanism.METHODS:After SGC-7901 cells were treated with toxicarioside A at various concentrations(0.5,1.5,4.5,9.0 μg/mL) for 24 h or 48 h,cell viability was determined by 3-(4,5-dimethyl-thiazol-2-yl)-2,5-diphenyl2H-tetrazolium bromide assay,and the motility and invasion of tumor cells were assessed by the Transwell chamber assay.Immunofluorescence staining,reverse transcription polymerase chain reaction and Western blotting were performed to detect the expression of basic fibroblast growth factor(bFGF) and fibroblast growth factor receptor-1(FGFR1),and nuclear factorkappa B(NF-κB) activation was examined by electrophoretic mobility shift assay.RESULTS:The results showed that toxicarioside A was capable of reducing cell viability,inhibiting cell growth,and suppressing cell migration and invasion activities in a time-and dose-dependent manner in SGC-7901 cells.Further analysis revealed that not only the expression of bFGF and its high-affinity receptor FGFR1 but also the NF-κB-DNA binding activity were effectively blocked by toxicarioside A in a dose-dependent manner compared with the control group(P < 0.05 or P < 0.01).Interestingly,application of the NF-κB specific inhibitor,pyrrolidinedithiocarbamate(PDTC),to SGC-7901 cells significantly potentized the toxicarioside A-induced down-regulation of bFGF compared with the control group(P < 0.05).CONCLUSION:These findings suggest that toxicarioside A has an anti-gastric cancer activity and this effect may be achieved partly through down-regulation of NF-κB and bFGF/FGFR1 signaling. 展开更多
关键词 Anti-migration ANTI-PROLIFERATION Basic fibroblast growth factor Gastric cancer Nuclear factorkappa B Toxicarioside A
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Immunotherapy of hepatoma with a monoclonal antibody against murine endoglin 被引量:3
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作者 guang-hong tan Feng-Ying Huang +3 位作者 Hua Wang Yong-Hao Huang Ying-Ying Lin Yue-Nan Li 《World Journal of Gastroenterology》 SCIE CAS CSCD 2007年第17期2479-2483,共5页
AIM: To explore the capability of a monoclonal antibody (mAb) against murine endoglin to inhibit tumor angiogenesis and suppression of hepatoma growth in murine models. METHODS: A monoclonal antibody against murine en... AIM: To explore the capability of a monoclonal antibody (mAb) against murine endoglin to inhibit tumor angiogenesis and suppression of hepatoma growth in murine models. METHODS: A monoclonal antibody against murine endoglin was purified by affinity chromatography and passively transfused through tail veins in two murine hepatoma models. Tumor volume and survival time were observed at three-day intervals for 48 d. Microvessels in tumor tissues were detected by immunohistochemistry against CD31, and angiogenesis in vivo was determined by alginate encapsulated assay. In addition, tumor cell apoptosis was detected by TUNEL assay. RESULTS: Passive immunotherapy with anti-endoglin mAb could effectively suppress tumor growth, and prolonged the survival time of hepatoma-bearing mice. Angiogenesis was apparently inhibited within the tumor tissues, and the vascularization of alginate beads was also reduced in the mice passively transfused with anti- endoglin mAb. In addition, increased apoptotic cells were observed within the tumor tissues from the mice passively transfused with anti-endoglin mAb. CONCLUSION: Passive immunotherapy with anti- endoglin mAb effectively inhibits tumor growth via inhibiting tumor angiogenesis and increasing tumor cell apoptosis, which may be highly correlated with the blockage of endoglin-related signal pathway induced bya nti-endoglin mAb. 展开更多
关键词 Monoclonal antibody ENDOGLIN Passive immunotherapy Tumor angiogenesis APOPTOSIS
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Toxicarioside A,isolated from tropical Antiaris toxicaria,blocks endoglin/TGF-βsignaling in a bone marrow stromal cell line
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作者 Yue-Nan Li Feng-Ying Huang +4 位作者 Wen-Li Mei Hao-Fu Dai Jun-Li Guo guang-hong tan Peng Zhou 《Asian Pacific Journal of Tropical Medicine》 SCIE CAS 2012年第2期91-97,共7页
Objective:To investigate possible mechanism of toxicarioside A in HS-5 bone stromal cells.Methods:HS-5 bone stromal cells were cultured in media supplemented with various concentrations of toxicarioside A or control D... Objective:To investigate possible mechanism of toxicarioside A in HS-5 bone stromal cells.Methods:HS-5 bone stromal cells were cultured in media supplemented with various concentrations of toxicarioside A or control DMSO(not treatment).Endoglin and TGF-βwere detected by Northern and Western blot analysis and quantified in a standard method. Downstream molecules of endoglin and TGF-β(Smad1,Smad2 and their active phosphorylated counterparts,pSmad1 and pSmad2) were also detected and quantified by Western blot analysis. In addition,cell proliferation assay and small interfering RNA(siRNA) against endoglin were used to certificate the function of endolgin in the HS-5 cells.Results:Compared with the not treated(0μg/mL) or DMSO treated control HS-5 cells,HS-5 cells treated with toxicarioside A were found significant attenuation of endolgin and TGF-βexpression.Significant inhibition of cell proliferation was also found in the HS-5 cells treated with toxicarioside A.ALK1-related Smad1 and ALK5-related Smad2 were decreased in HS-5 cells treated with toxicarioside A.In addition,phosphorylated Smad1(pSmad1) and Smad2(pSmad2) were also found attenuation in toxicarioside A-treated HS-5 cells.RNA interference showed that blockage of endoglin by siRNA also decreased Smad1 and Smad2 expression in HS-5 cells.Conclusions:Our results indicate that toxicarioside A can influence bone marrow stromal HS-5’s function and inhibit HS-5 cell proliferation by alteration of endoglin-related ALK1(Smad1) and ALK5(Smad2) signaling. 展开更多
关键词 Toxicarioside A ENDOGLIN TRANSFORMING growth factor-β Signal pathway Cell PROLIFERATION
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Cytochalasin D,a tropical fungal metabolite,inhibits CT26 tumor growth and angiogenesis
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作者 Feng-Ying Huang Yue-Nan Li +3 位作者 Wen-Li Mei Hao-Fu Dai Peng Zhou guang-hong tan 《Asian Pacific Journal of Tropical Medicine》 SCIE CAS 2012年第3期169-174,共6页
Objective:To investigate whether eytochalasin D can induce antitumor activities in a tumor model.Methods:Murine CT26 colorectal carcinoma cells were cultured hi vitro and cytochalasin D was used as a cytotoxic agent t... Objective:To investigate whether eytochalasin D can induce antitumor activities in a tumor model.Methods:Murine CT26 colorectal carcinoma cells were cultured hi vitro and cytochalasin D was used as a cytotoxic agent to detect its capabilities of inhibiting CT26 cell proliferation and inducing cell apoptosis by MTT and a TUNEL-based apoptosis assay.Murine CT26 tumor model was established to observe the tumor growth and survival time.Tumor tissues were used to detect the mierovessel density by immunohistochemistry.In addition,alginate encapsulated tumor cell assay was used to quantify the tumor angiogenesis in vivo.Results:Cytochalasin D inhibited CT26 tumor cell proliferation in lime and dose dependent manner and induced signiflcanl CT26 cell apoptosis,which almost reached the level induced by the positive control nuclease.The optimum effective dose of cytochalasin D for in vivo therapy was about 50 mg/kg.Cytochalasin D in vivo treatment significandy inhibited tumor growth and prolonged the survival times in CT26 tumor-bearing mice.The results of immunohistochemistry analysis and alginate encapsulation assay indicated that the cytochalasin D could effectively inhibited tumor angiogenesis. Conclusions:Cytochalasin D inhibits CT26 tumor growth potentially through inhibition of cell proliferation,induction of cell apoptosis and suppression of tumor angiogenesis. 展开更多
关键词 CYTOCHALASIN D CT26 COLORECTAL carcinoma Apoptosis Tumor ANGIOGENESIS
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The Non-Coding RNA Llme23 Drives the Malignant Property of Human Melanoma Cells 被引量:6
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作者 Chuan-Fang Wu guang-hong tan +1 位作者 Cheng-Chuan Ma Ling Li 《Journal of Genetics and Genomics》 SCIE CAS CSCD 2013年第4期179-188,共10页
Several lines of evidence support the notion that increased RNA-binding ability of polypyrimidine tract-binding(PTB) proteinassociated splicing factor(PSF) and aberrant expression of long non-coding RNAs(IncRNAs... Several lines of evidence support the notion that increased RNA-binding ability of polypyrimidine tract-binding(PTB) proteinassociated splicing factor(PSF) and aberrant expression of long non-coding RNAs(IncRNAs) are associated with mouse and human tumors.To identify the PSF-binding IncRNA involved in human oncogenesis,we screened a nuclear RNA repertoire of human melanoma cell line,YUSAC,through RNA-SELEX affinity chromatography.A previously unreported IncRNA,termed as Llme23,was found to bind immobilized PSF resin.The specific binding of Llme23 to both recombinant and native PSF protein was confirmed in vitro and in vivo. The expression of PSF-binding Llme23 is exclusively detected in human melanoma lines.Knocking down Llme23 remarkably suppressed the malignant property of YUSAC cells,accompanied by the repressed expression of proto-oncogene Rab23.These results may indicate that Llme23 can function as an oncogenic RNA and directly associate the PSF-binding IncRNA with human melanoma. 展开更多
关键词 LncRNA Llme23 PSF MELANOMA Rab23
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