柯里拉京通过下调NOTCH1信号通路抑制胃癌SGC-7901细胞增殖的实验研究
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摘要
目的探讨柯里拉京能否通过下调NOTCH1信号通路抑制胃癌SGC-7901细胞的增殖,以及对Hes1表达的影响。方法使用不同浓度的柯里拉京(0μg/ml、10μg/ml和100μg/ml)对胃癌SGC-7901细胞进行干预。在不同时间点(0、24和48h)使用MTT法对SGC-7901细胞活性进行检测。干预48h后,使用qPCR和western blot对在不同浓度(0μg/ml、10μg/ml和100μg/ml)柯里拉京干预后,细胞NOTCH1、Hes1mRNA和蛋白的表达水平进行分析。结果使用不同浓度柯里拉京(0μg/ml、10μg/ml和100μg/ml)对胃癌SGC-7901细胞进行干预后,细胞活性呈时间依赖性和剂量依赖性下降,差异均有统计学意义(P<0.05)。不同浓度柯里拉京(0μg/ml、10μg/ml和100μg/ml)干预48h后,胃癌SGC-7901细胞NOTCH1及Hes1 mRNA和蛋白的表达水平呈剂量依赖性降低,差异均有统计学意义(P<0.05)。结论柯里拉京可通过下调NOTCH1/Hes1信号通路抑制胃癌SGC-7901细胞增殖,同时为柯里拉京用于临床治疗胃癌等恶性肿瘤奠定了实验基础。
Objective To explore whether corilagin would suppress the proliferation of gastric cancer SGC-7901 cells through mediation of NOTCH1/Hes1 pathway.Methods Three different concentrations(0μg/ml,10μg/ml and100μg/ml)of corilagin were obtained in our study.At different time points(0 h,24 hand 48 h),MTT assay was used to analyze the cell viabilities.QPCR was used to measure NOTCH1 and Hes1 mRNA expression.Western blot was performed to analyze the protein expression of NOTCH1 and Hes1.Results The cell viabilities of gastric cancer SGC-7901 cells were concentration-dependently and time-dependently supressed by corilagin.Then,the mRNA and protein expression of NOTCH1 and Hes1 were also concentration-dependently inhibited by corilagin in gastric cancer SGC-7901 cells,after 48 hof intervention.Conclusion Corilagin could suppress the proliferation of gastric cancer SGC-7901 cells through down-regulation of NOTCH1/Hes1 signal pathway.
Objective To explore whether corilagin would suppress the proliferation of gastric cancer SGC-7901 cells through mediation of NOTCH1/Hes1 pathway.Methods Three different concentrations(0μg/ml,10μg/ml and100μg/ml)of corilagin were obtained in our study.At different time points(0 h,24 hand 48 h),MTT assay was used to analyze the cell viabilities.QPCR was used to measure NOTCH1 and Hes1 mRNA expression.Western blot was performed to analyze the protein expression of NOTCH1 and Hes1.Results The cell viabilities of gastric cancer SGC-7901 cells were concentration-dependently and time-dependently supressed by corilagin.Then,the mRNA and protein expression of NOTCH1 and Hes1 were also concentration-dependently inhibited by corilagin in gastric cancer SGC-7901 cells,after 48 hof intervention.Conclusion Corilagin could suppress the proliferation of gastric cancer SGC-7901 cells through down-regulation of NOTCH1/Hes1 signal pathway.
引文
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[2]Liu KT,Wan JF,Yu GH,et al.The recommended treatment strategy for locally advanced gastric cancer in elderly patients aged 75years and older:a Surveillance,Epidemiology,and End Results database analysis[J].J Cancer Res Clin Oncol,2017,143(2):313-320.
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[5]杨文涛,李正友,于喜贞,等.柯里拉京对神经胶质瘤U251细胞及其干细胞增殖的影响[J].中国微侵袭神经外科杂志,2015,20(12):564-568.
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[8]尹鹏,胡君,储著凌,等.γ-分泌酶抑制剂DAPT通过下调NOTCH1信号通路抑制结肠癌HCT116细胞增殖的实验研究[J].西部医学,2015,27(11):1616-1619.doi:10.3969/j.issn.1672-3511.2015.11.005
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[12]Zhu T,Wu XL,Zhang W,et al.Glucagon Like Peptide-1(GLP-1)Modulates OVA-Induced Airway Inflammation and Mucus Secretion Involving a Protein Kinase A(PKA)-Dependent Nuclear Factor-κB(NF-κB)Signaling Pathway in Mice[J].Int J Mol Sci,2015,16(9):20195-20211.
[13]Zhu T,Wang DX,Zhang W,et al.Andrographolide Protects Against LPS-induced Acute Lung Injury by Inactivation of NF-κB[J].PLOS ONE,2013,8(2):e56407.
[14]姚健,桑晓梅,罗黔.3D高清腹腔镜手术的临床应用探讨[J].西部医学,2013,25(4):513-514.
[15]王宝华,王宁,冯雅靖,等.1990年与2013年中国人群胃癌疾病负担分析[J].中华流行病学杂志,2016,37(006):763-767.
[16]Gu Y,Xiao L,Ming Y,et al.Corilagin suppresses cholangiocarcinoma progression through Notch signaling pathway in vitro and in vivo[J].Int J Oncol,2016,48(5):1868-1876.
[17]Jia L1,Jin H,Zhou J,et al.A potential anti-tumor herbal medicine,Corilagin,inhibits ovarian cancer cell growth through blocking the TGF-βsignaling pathways[J].BMC Complement Altern Med,2013,13:33.
[18]Sawaguchi S,Varshney S,Ogawa M,et al.O-GlcNAc on NOTCH1EGF repeats regulates ligand-induced Notch signaling and vascular development in mammals[J].Elife,2017,6:e24419.
[19]Zhou Y,Liao S,Zhang Z,et al.Astragalus injection attenuates bleomycin-induced pulmonary fibrosis via down-regulating Jagged1/Notch1in lungs[J].J Pharm Pharmacol,2016,68(3):389-396.
[20]Li Y,Zhang T,Zhou Y,et al.A Presenilin/Notch1pathway regulated by miR-375,miR-30a,and miR-34a mediates glucotoxicity induced-pancreatic beta cell apoptosis[J].Sci Rep,2016,6:36136.
[21]Batchuluun K,Azuma M,Fujiwara K,et al.Notch Signaling and Maintenance of SOX2Expression in Rat Anterior Pituitary Cells[J].Acta Histochem Cytochem,2017,50(2):63-69.
[22]Zhang Q,Wang C,Liu Z,et al.Notch signal suppresses Tolllike receptor-triggered inflammatory responses in macrophages by inhibiting extracellular signal-regulated kinase 1/2-mediated nuclear factorκB activation[J].J Biol Chem,2012,287(9):6208-6217.
[2]Liu KT,Wan JF,Yu GH,et al.The recommended treatment strategy for locally advanced gastric cancer in elderly patients aged 75years and older:a Surveillance,Epidemiology,and End Results database analysis[J].J Cancer Res Clin Oncol,2017,143(2):313-320.
[3]Moss SF.The Clinical Evidence Linking Helicobacter pylori to Gastric Cancer[J].Cell Mol Gastroenterol Hepatol,2016,3(2):183-191.
[4]张军,李林均,王亚萍,等.替吉奥联合奥沙利铂治疗晚期及复发性胃癌的临床观察[J].西部医学,2010,22(12):2228-2230.
[5]杨文涛,李正友,于喜贞,等.柯里拉京对神经胶质瘤U251细胞及其干细胞增殖的影响[J].中国微侵袭神经外科杂志,2015,20(12):564-568.
[6]黄艺芬,陈盛铎,王月凤,等.柯里拉京对血吸虫病小鼠肝组织白细胞介素-13表达的影响及其抗肝纤维化疗效研究[J].中西医结合肝病杂志,2011,21(3):156-158.
[7]陈一燕,陈崇宏.柯里拉京药理活性研究进展[J].中国现代应用药学,2010,27(5):390-394.
[8]尹鹏,胡君,储著凌,等.γ-分泌酶抑制剂DAPT通过下调NOTCH1信号通路抑制结肠癌HCT116细胞增殖的实验研究[J].西部医学,2015,27(11):1616-1619.doi:10.3969/j.issn.1672-3511.2015.11.005
[9]Kang JA,Kim WS,Park SG.Notch1is an important mediator for enhancing of B-cell activation and antibody secretion by Notch ligand[J].Immunology,2014,143(4):550-559.
[10]谷乐,李文岗,胡素贤.柯里拉京对人肺腺癌细胞增殖和Notch信号通路的影响[J].中华实验外科杂志,2014,31(011):2483-2485.
[11]Zhu T,Zhang W,Feng SJ,et al.Emodin suppresses LPS-induced inflammation in RAW264.7cells through a PPARγ-dependent pathway[J].Int Immunopharmacol,2016,34:16-24.
[12]Zhu T,Wu XL,Zhang W,et al.Glucagon Like Peptide-1(GLP-1)Modulates OVA-Induced Airway Inflammation and Mucus Secretion Involving a Protein Kinase A(PKA)-Dependent Nuclear Factor-κB(NF-κB)Signaling Pathway in Mice[J].Int J Mol Sci,2015,16(9):20195-20211.
[13]Zhu T,Wang DX,Zhang W,et al.Andrographolide Protects Against LPS-induced Acute Lung Injury by Inactivation of NF-κB[J].PLOS ONE,2013,8(2):e56407.
[14]姚健,桑晓梅,罗黔.3D高清腹腔镜手术的临床应用探讨[J].西部医学,2013,25(4):513-514.
[15]王宝华,王宁,冯雅靖,等.1990年与2013年中国人群胃癌疾病负担分析[J].中华流行病学杂志,2016,37(006):763-767.
[16]Gu Y,Xiao L,Ming Y,et al.Corilagin suppresses cholangiocarcinoma progression through Notch signaling pathway in vitro and in vivo[J].Int J Oncol,2016,48(5):1868-1876.
[17]Jia L1,Jin H,Zhou J,et al.A potential anti-tumor herbal medicine,Corilagin,inhibits ovarian cancer cell growth through blocking the TGF-βsignaling pathways[J].BMC Complement Altern Med,2013,13:33.
[18]Sawaguchi S,Varshney S,Ogawa M,et al.O-GlcNAc on NOTCH1EGF repeats regulates ligand-induced Notch signaling and vascular development in mammals[J].Elife,2017,6:e24419.
[19]Zhou Y,Liao S,Zhang Z,et al.Astragalus injection attenuates bleomycin-induced pulmonary fibrosis via down-regulating Jagged1/Notch1in lungs[J].J Pharm Pharmacol,2016,68(3):389-396.
[20]Li Y,Zhang T,Zhou Y,et al.A Presenilin/Notch1pathway regulated by miR-375,miR-30a,and miR-34a mediates glucotoxicity induced-pancreatic beta cell apoptosis[J].Sci Rep,2016,6:36136.
[21]Batchuluun K,Azuma M,Fujiwara K,et al.Notch Signaling and Maintenance of SOX2Expression in Rat Anterior Pituitary Cells[J].Acta Histochem Cytochem,2017,50(2):63-69.
[22]Zhang Q,Wang C,Liu Z,et al.Notch signal suppresses Tolllike receptor-triggered inflammatory responses in macrophages by inhibiting extracellular signal-regulated kinase 1/2-mediated nuclear factorκB activation[J].J Biol Chem,2012,287(9):6208-6217.