[Objectives]To observe the effect of drug-containing serum from different extracts of Phyllanthus reticulatus leaf on the proliferation of human gastric cancer SGC-7901 cells and the effect of in vivo on the life exte...[Objectives]To observe the effect of drug-containing serum from different extracts of Phyllanthus reticulatus leaf on the proliferation of human gastric cancer SGC-7901 cells and the effect of in vivo on the life extension rate of mice with H22 ascites tumor,and to investigate the effects of chemical components such as Corilagin,ethyl gallate,ethyl brevifolincarboxylate,and gallic acid on the proliferation of human gastric cancer SGC-7901 cells.[Methods]MTT method was used to observe the inhibitory effect of drug-containing serum of different extracts of P.reticulatus leaf on human gastric cancer SGC-7901 cells in vitro to determine its active site.The active site was used as the research object to establish a Kunming mouse ascites tumor model,to investigate the effect on the life extension rate of mice with H22 ascites tumor,to further separate the monomer components from the effective fraction and investigate its effect on human gastric cancer SGC-7901 cells.[Results]Compared with the 10%blank serum control group,10%drug-containing serum of ethyl acetate and n-butanol in P.reticulatus leaf had significant inhibitory effect on the proliferation of human gastric cancer SGC-7901 cells,and the inhibition rate was 34.99%and 28.68%,respectively(P<0.05).Compared with the blank group,the survival time of the high dose group of ethyl acetate in P.reticulatus leaf was significant(P<0.05).Gallic acid,Corilagin,and Brevifolincarboxylic acid ethyl ester had a significant inhibitory effect on the proliferation of human gastric cancer SGC-7901 cells,with IC 50 of 26.52,70.45,and 158.86μg/mL,respectively.Ethyl gallate had no inhibitory effect on the proliferation of human gastric cancer SGC-7901 cells,and its IC 50 was 251.96μg/mL.[Conclusions]The drug-containing serum of ethyl acetate and n-butanol extract of P.reticulatus can inhibit the proliferation of human gastric cancer SGC-7901 cells.Ethyl acetate of P.reticulatus leaves can increase the life extension rate of mice with H22 ascites tumor.Gallic acid,Corilagin,and Brevifolincarboxylic acid ethyl ester isolated from its active site are the material basis for inhibiting the proliferation of human gastric cancer SGC-7901 cells.展开更多
Objective: To investigate the cytotoxic effects and the potential mechanisms of crebanine N-oxide in SGC-7901 gastric adenocarcinoma cells. Methods: The cytotoxicity of crebanine N-oxide was evaluated by 3-(4,5-dimeth...Objective: To investigate the cytotoxic effects and the potential mechanisms of crebanine N-oxide in SGC-7901 gastric adenocarcinoma cells. Methods: The cytotoxicity of crebanine N-oxide was evaluated by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide assay and cellular morphology was observed under a microscope. Cell apoptosis was determined by flow cytometry using propidium iodide staining. The expression levels of apoptotic-related proteins, cleaved caspase-3, cytochrome C, p53 and Bax, and autophagyrelated proteins p62, beclin1 and LC3 were detected by Western blotting assays. Results: Crebanine N-oxide treatment significantly inhibited the proliferation of SGC-7901 cells in a dose-dependent and timedependent manner via induction of G2-phase cell cycle arrest, apoptosis, and autophagy in SGC-7901 cells.Conclusions: Crebanine N-oxide could inhibit the growth of gastric cancer cells by promoting apoptosis and autophagy and could be used as a potential agent for treating gastric cancer.展开更多
AIM: To investigate the low intensity ultrasound (US)-induced apoptosis in human gastric carcinoma cells and its potential mechanism and to suggest a new therapeutic approach to gastric carcinoma. METHODS: Human SGC-7...AIM: To investigate the low intensity ultrasound (US)-induced apoptosis in human gastric carcinoma cells and its potential mechanism and to suggest a new therapeutic approach to gastric carcinoma. METHODS: Human SGC-7901 gastric carcinoma cells were cultured in vitro and irradiated by low intensity US for 10 min at different intensities with different incubation times after irradiation. Morphologic changes were examined under microscope with trypan blue staining and then the percentage of early apoptotic cells was detected by flow cytometry (FCM) with double staining of fluorescein isothiocyanate (FITC)-Annexin V/propidium iodide (PI). Two-dimensional electrophoresis (2DE) was used to get the protein profile and some proteins differently expressed after US irradiation were identifi ed by matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF-MS). Functional analysis was performed to investigate the mechanism of US-induced cell apoptosis. RESULTS: The percentage of apoptotic cells increased about 10% after US irradiation (12.0 W/cm^2, 12 h culture). The percentage of early apoptosis and secondary necrosis in the US-irradiated cells increased with the increased US intensity. Moreover, apoptotic cells increased with the increased culture time after US irradiation and reached its maximum at about 12 h.Several new proteins appeared after US irradiation and were up or down regulated more than 2 times. Some heat shock proteins (HSPs) were found to be associated with the signal process simulating the apoptosis of cells. CONCLUSION: Low intensity US could induce apoptosis in human gastric carcinoma cells. US-induced apoptosis is related to US intensity/culture time. US-induced apoptosis may be caspases-dependent and endoplasmic reticulum (ER) stress-triggered apoptosis may also contribute to it. Proteomic experimental system is useful in finding the protein alteration in carcinoma cells after US irradiation, helping to develop a new cancer therapy.展开更多
Recent observations indicate that the resistance of apoptosis is an important process of tumor metastasis and metastases are the cause of 90% of human cancer death. Etoposide, a semisynthetic derivative of the podophy...Recent observations indicate that the resistance of apoptosis is an important process of tumor metastasis and metastases are the cause of 90% of human cancer death. Etoposide, a semisynthetic derivative of the podophyllotoxins, is a clinically used anti-cancer reagent, but the effects of it on metastatic gastric carcinoma cells are totally unknown. In this study, etoposide induced apoptotic cell death in human gastric adenocarcinoma cell line SGC-7901, derived from metastatic lymph nodes, as evidenced by the analysis of DNA fragmentation, apoptotic body formation, caspase activation, and apoptosis specific changes in cell morphology is demonstrated. The depolarization of mitochondrial membrane and the release of cytochrome c were most early events in etoposide treated SGC-7901 cells, and were followed by caspase-3 activation and PARP cleavage. Caspase-8 activation was not detected under the same condition. Thus, it was proposed that etoposide induces caspase-associated apoptotic cell death in human metastatic gastric carcinoma, which is initiated by mitochondrial cytochrome c release.展开更多
AIM: To investigate the growth effects of 4-phenyl butyric acid (PBA) on human gastric carcinoma cells and their mechanisms. METHODS: Moderately-differentiated human gastric carcinoma SGC-7901 and lowly-differentiated...AIM: To investigate the growth effects of 4-phenyl butyric acid (PBA) on human gastric carcinoma cells and their mechanisms. METHODS: Moderately-differentiated human gastric carcinoma SGC-7901 and lowly-differentiated MGC-803 cells were treated with 5, 10, 20, 40, and 60 μmol/L PBA for 1-4 d. Cell proliferation was detected using the MTT colorimetric assay. Cell cycle distributions were examined using flow cytometry.RESULTS: The proliferation of gastric carcinoma cells was inhibited by PBA in a doseand time-dependent fashion. Flow cytometry showed that SGC-7901 cells treated with low concentrations of PBA were arrested at the G0/G1 phase, whereas cells treated with high concentrations of PBA were arrested at the G2/M phase. Although MGC-803 cells treated with low concentrations of PBA were also arrested at the G0/G1 phase, cells treated with high concentrations of PBA were arrested at the S phase. CONCLUSION: The growth inhibitory effect of PBA on gastric cancer cells is associated with alteration of the cell cycle. For moderately-differentiated gastric cancer cells, the cell cycle was arrested at the G0/G1 and G2/M phases. For lowly-differentiated gastric cancer cells, the cell cycle was arrested at the G0/G1 and S phases.展开更多
Objective: To research the inhibitory effect on SGC-7901 cells of α-pinene, and the related mechanism of α-pinene. Methods: Used the MTT method to detect inhibition rate and western blotting to detect the influence ...Objective: To research the inhibitory effect on SGC-7901 cells of α-pinene, and the related mechanism of α-pinene. Methods: Used the MTT method to detect inhibition rate and western blotting to detect the influence on expression of ATM, Phos-S1981ATM, H2AX, γH2AX, CHK2 and p-CHK2, p53 and phos-p53 cell cycle related protein in SGC-7901 cells. Results: The research found α-pinene could inhibit the proliferation of SGC-7901 cells observably in vitro, and the inhibition rate assumes the dependence on concentration;and western blotting results showed that, α-pinene could activate phospho-ATM, increase the amount of γH2AX (p p < 0.05);increase the expression of p-CHK2, p53 and phos-p53 (p p p < 0.05);But there is no significant effect on expression of CHK2 (p > 0.05). Conclusions: α-pinene could inhibit the proliferation of SGC-7901 cells, and by inducing ATM (Ataxia Telangiectasia-Mutated) kinase signal pathway in DNA damage response, activating cell cycle checkpoint, making the cell cycle arrest then exerts its anti-tumor effects.展开更多
目的通过测定隐丹参酮对人胃癌SGC-7901细胞增殖及血管内皮生长因子(VEGF)mRNA的影响,探讨其抗肿瘤的作用机制。方法采用四甲基偶氮唑蓝(MTT)比色法检测隐丹参酮对人胃癌SGC-7901细胞增殖的影响,采用Real Time RT-PCR检测隐丹参酮对...目的通过测定隐丹参酮对人胃癌SGC-7901细胞增殖及血管内皮生长因子(VEGF)mRNA的影响,探讨其抗肿瘤的作用机制。方法采用四甲基偶氮唑蓝(MTT)比色法检测隐丹参酮对人胃癌SGC-7901细胞增殖的影响,采用Real Time RT-PCR检测隐丹参酮对VEGF m RNA表达的影响。结果 20、40、60、80、100μmol/L的隐丹参酮作用于人胃癌SGC-7901细胞6-48 h,其生长和增殖均受到一定程度的抑制;24 h为隐丹参酮对SGC-7901细胞抑制作用的最佳时间,IC50为59.11μmol/L;选取40、60和80μmol/L 3个剂量作用于人胃癌细胞SGC7901 24 h后,60和80μmol/L的隐丹参酮均可下调VEGF m RNA的表达(均P〈0.01)。结论隐丹参酮可抑制人胃癌SGC-7901细胞增殖,并能抑制VEGF mRNA的表达,提示这可能是其抗肿瘤的作用机制之一。展开更多
基金Supported by Natural Science Research Project of Guangxi University of Chinese Medicine in 2015"Study on Anti-tumor Effect of Phyllanthus reticulatus Leaf Extract"(p15028)Independent Research Program of Guangxi Key Laboratory of Traditional Chinese Medicine Pharmacology in 2015"Study on Phyllanthus reticulatus Leaf 7404 Nude Mice Xenografts"+1 种基金Young Teachers Enhancement Project of Guangxi Department of Education in 2018"Study on the Mechanism of Zhuang Medicine Phyllanthus reticulatus Leaf against Liver Cancer"(2018KY0300)2019-2021 Guangxi First-class Discipline Construction Open Project Fund for Young Scholars of Guangxi University of Chinese Medicine"Anti-hepatocarcinoma Mechanism of Autophagy Induced by Ethyl Acetate in Phyllanthus reticulatus Leaf Based on PI3K/AKT and STAT3/m TOR Signaling Pathway"(2019XK089)
文摘[Objectives]To observe the effect of drug-containing serum from different extracts of Phyllanthus reticulatus leaf on the proliferation of human gastric cancer SGC-7901 cells and the effect of in vivo on the life extension rate of mice with H22 ascites tumor,and to investigate the effects of chemical components such as Corilagin,ethyl gallate,ethyl brevifolincarboxylate,and gallic acid on the proliferation of human gastric cancer SGC-7901 cells.[Methods]MTT method was used to observe the inhibitory effect of drug-containing serum of different extracts of P.reticulatus leaf on human gastric cancer SGC-7901 cells in vitro to determine its active site.The active site was used as the research object to establish a Kunming mouse ascites tumor model,to investigate the effect on the life extension rate of mice with H22 ascites tumor,to further separate the monomer components from the effective fraction and investigate its effect on human gastric cancer SGC-7901 cells.[Results]Compared with the 10%blank serum control group,10%drug-containing serum of ethyl acetate and n-butanol in P.reticulatus leaf had significant inhibitory effect on the proliferation of human gastric cancer SGC-7901 cells,and the inhibition rate was 34.99%and 28.68%,respectively(P<0.05).Compared with the blank group,the survival time of the high dose group of ethyl acetate in P.reticulatus leaf was significant(P<0.05).Gallic acid,Corilagin,and Brevifolincarboxylic acid ethyl ester had a significant inhibitory effect on the proliferation of human gastric cancer SGC-7901 cells,with IC 50 of 26.52,70.45,and 158.86μg/mL,respectively.Ethyl gallate had no inhibitory effect on the proliferation of human gastric cancer SGC-7901 cells,and its IC 50 was 251.96μg/mL.[Conclusions]The drug-containing serum of ethyl acetate and n-butanol extract of P.reticulatus can inhibit the proliferation of human gastric cancer SGC-7901 cells.Ethyl acetate of P.reticulatus leaves can increase the life extension rate of mice with H22 ascites tumor.Gallic acid,Corilagin,and Brevifolincarboxylic acid ethyl ester isolated from its active site are the material basis for inhibiting the proliferation of human gastric cancer SGC-7901 cells.
基金supported by the National Natural Science Foundation of China(NO.81760628).
文摘Objective: To investigate the cytotoxic effects and the potential mechanisms of crebanine N-oxide in SGC-7901 gastric adenocarcinoma cells. Methods: The cytotoxicity of crebanine N-oxide was evaluated by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide assay and cellular morphology was observed under a microscope. Cell apoptosis was determined by flow cytometry using propidium iodide staining. The expression levels of apoptotic-related proteins, cleaved caspase-3, cytochrome C, p53 and Bax, and autophagyrelated proteins p62, beclin1 and LC3 were detected by Western blotting assays. Results: Crebanine N-oxide treatment significantly inhibited the proliferation of SGC-7901 cells in a dose-dependent and timedependent manner via induction of G2-phase cell cycle arrest, apoptosis, and autophagy in SGC-7901 cells.Conclusions: Crebanine N-oxide could inhibit the growth of gastric cancer cells by promoting apoptosis and autophagy and could be used as a potential agent for treating gastric cancer.
基金The National Natural Science Foundation of China (No. 30630024)the Key Project of Ministry of Education (No. 705046)the Doctoral Foundation of Xi’an Jiaotong University (grants No. DFXJTU2005-05)
文摘AIM: To investigate the low intensity ultrasound (US)-induced apoptosis in human gastric carcinoma cells and its potential mechanism and to suggest a new therapeutic approach to gastric carcinoma. METHODS: Human SGC-7901 gastric carcinoma cells were cultured in vitro and irradiated by low intensity US for 10 min at different intensities with different incubation times after irradiation. Morphologic changes were examined under microscope with trypan blue staining and then the percentage of early apoptotic cells was detected by flow cytometry (FCM) with double staining of fluorescein isothiocyanate (FITC)-Annexin V/propidium iodide (PI). Two-dimensional electrophoresis (2DE) was used to get the protein profile and some proteins differently expressed after US irradiation were identifi ed by matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF-MS). Functional analysis was performed to investigate the mechanism of US-induced cell apoptosis. RESULTS: The percentage of apoptotic cells increased about 10% after US irradiation (12.0 W/cm^2, 12 h culture). The percentage of early apoptosis and secondary necrosis in the US-irradiated cells increased with the increased US intensity. Moreover, apoptotic cells increased with the increased culture time after US irradiation and reached its maximum at about 12 h.Several new proteins appeared after US irradiation and were up or down regulated more than 2 times. Some heat shock proteins (HSPs) were found to be associated with the signal process simulating the apoptosis of cells. CONCLUSION: Low intensity US could induce apoptosis in human gastric carcinoma cells. US-induced apoptosis is related to US intensity/culture time. US-induced apoptosis may be caspases-dependent and endoplasmic reticulum (ER) stress-triggered apoptosis may also contribute to it. Proteomic experimental system is useful in finding the protein alteration in carcinoma cells after US irradiation, helping to develop a new cancer therapy.
基金the National Natural Science Foundation of China(Nos.30640064 and 30770447).
文摘Recent observations indicate that the resistance of apoptosis is an important process of tumor metastasis and metastases are the cause of 90% of human cancer death. Etoposide, a semisynthetic derivative of the podophyllotoxins, is a clinically used anti-cancer reagent, but the effects of it on metastatic gastric carcinoma cells are totally unknown. In this study, etoposide induced apoptotic cell death in human gastric adenocarcinoma cell line SGC-7901, derived from metastatic lymph nodes, as evidenced by the analysis of DNA fragmentation, apoptotic body formation, caspase activation, and apoptosis specific changes in cell morphology is demonstrated. The depolarization of mitochondrial membrane and the release of cytochrome c were most early events in etoposide treated SGC-7901 cells, and were followed by caspase-3 activation and PARP cleavage. Caspase-8 activation was not detected under the same condition. Thus, it was proposed that etoposide induces caspase-associated apoptotic cell death in human metastatic gastric carcinoma, which is initiated by mitochondrial cytochrome c release.
基金Supported by Natural Science Foundation of Ningbo, No. 2009A610134Natural Sciences Foundation of Zhejiang, No. Y207244+3 种基金College Students’ Science-Technology Innovation Program of Zhejiang Province, No. 200959the Excellent Disser-tation Foundation of Ningbo University, No. 201014KC Wong Magna Fund of Ningbo Universitythe Scientific Innovation Team Project of Ningbo, No.2011B82014
文摘AIM: To investigate the growth effects of 4-phenyl butyric acid (PBA) on human gastric carcinoma cells and their mechanisms. METHODS: Moderately-differentiated human gastric carcinoma SGC-7901 and lowly-differentiated MGC-803 cells were treated with 5, 10, 20, 40, and 60 μmol/L PBA for 1-4 d. Cell proliferation was detected using the MTT colorimetric assay. Cell cycle distributions were examined using flow cytometry.RESULTS: The proliferation of gastric carcinoma cells was inhibited by PBA in a doseand time-dependent fashion. Flow cytometry showed that SGC-7901 cells treated with low concentrations of PBA were arrested at the G0/G1 phase, whereas cells treated with high concentrations of PBA were arrested at the G2/M phase. Although MGC-803 cells treated with low concentrations of PBA were also arrested at the G0/G1 phase, cells treated with high concentrations of PBA were arrested at the S phase. CONCLUSION: The growth inhibitory effect of PBA on gastric cancer cells is associated with alteration of the cell cycle. For moderately-differentiated gastric cancer cells, the cell cycle was arrested at the G0/G1 and G2/M phases. For lowly-differentiated gastric cancer cells, the cell cycle was arrested at the G0/G1 and S phases.
文摘Objective: To research the inhibitory effect on SGC-7901 cells of α-pinene, and the related mechanism of α-pinene. Methods: Used the MTT method to detect inhibition rate and western blotting to detect the influence on expression of ATM, Phos-S1981ATM, H2AX, γH2AX, CHK2 and p-CHK2, p53 and phos-p53 cell cycle related protein in SGC-7901 cells. Results: The research found α-pinene could inhibit the proliferation of SGC-7901 cells observably in vitro, and the inhibition rate assumes the dependence on concentration;and western blotting results showed that, α-pinene could activate phospho-ATM, increase the amount of γH2AX (p p < 0.05);increase the expression of p-CHK2, p53 and phos-p53 (p p p < 0.05);But there is no significant effect on expression of CHK2 (p > 0.05). Conclusions: α-pinene could inhibit the proliferation of SGC-7901 cells, and by inducing ATM (Ataxia Telangiectasia-Mutated) kinase signal pathway in DNA damage response, activating cell cycle checkpoint, making the cell cycle arrest then exerts its anti-tumor effects.
文摘目的通过测定隐丹参酮对人胃癌SGC-7901细胞增殖及血管内皮生长因子(VEGF)mRNA的影响,探讨其抗肿瘤的作用机制。方法采用四甲基偶氮唑蓝(MTT)比色法检测隐丹参酮对人胃癌SGC-7901细胞增殖的影响,采用Real Time RT-PCR检测隐丹参酮对VEGF m RNA表达的影响。结果 20、40、60、80、100μmol/L的隐丹参酮作用于人胃癌SGC-7901细胞6-48 h,其生长和增殖均受到一定程度的抑制;24 h为隐丹参酮对SGC-7901细胞抑制作用的最佳时间,IC50为59.11μmol/L;选取40、60和80μmol/L 3个剂量作用于人胃癌细胞SGC7901 24 h后,60和80μmol/L的隐丹参酮均可下调VEGF m RNA的表达(均P〈0.01)。结论隐丹参酮可抑制人胃癌SGC-7901细胞增殖,并能抑制VEGF mRNA的表达,提示这可能是其抗肿瘤的作用机制之一。