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作 者:胡俊 李原[2] 黄培林[3] 魏青[4] 常立功[3] 胡明玥[3] 周玲娜[3] 申霞[3] 燕丹[4] Hu Jun Li Yuan Huang Peilin Wei Qin Chang Ligong Hu Mingyue Zhou Linna Shen Xia Yan Dan(Depantment of Oncology,Nanjing Red Cross Hospital,Nanjing 210001 Depantment of Oncology,the Second Hospital Affiliated to Southeast University, Nanjing 210003 JDepantment of Pathology,Medical College, Southeast University, Nanjing 21000 Depantment of Pharmacy, Jiangsu Cancer Hospital, Nanjing 210009, China)
机构地区:[1]南京红十字医院肿瘤科,江苏南京210001 [2]东南大学附属第二医院肿瘤科,江苏南京210003 [3]东南大学医学院病理学系,江苏南京210009 [4]江苏省肿瘤医院药剂科,江苏南京210009
出 处:《南京医科大学学报(自然科学版)》2016年第11期1295-1299,共5页Journal of Nanjing Medical University(Natural Sciences)
基 金:国家自然科学基金(81372152);北京医学奖励基金(YJHYXKYJJ-433);江苏省肿瘤医院青年基金(ZQ201503)
摘 要:目的 :锌α2糖脂蛋白(zinc-alpha-2-glycoprotein 1,ZAG)是新近发现的具有复杂功能的蛋白,ZAG参与受精、脂代谢及免疫调节等多种细胞生物学行为,本研究探讨ZAG在大肠癌演进过程中的作用。方法:本研究构建ZAG干扰质粒,并转染入HT-29结肠癌细胞株,免疫印迹与逆转录聚合酶链式反应(RT-PCR)方法检测转染前后ZAG表达的变化;检测转染前后细胞三磷酸腺苷(adenosine triphosphate,ATP)含量的变化,以了解ZAG对细胞代谢的影响;利用小室实验检测转染前后HT-29细胞侵袭能力的变化。结果:ZAG干扰质粒成功转染入HT-29细胞并筛选出稳定转染细胞株;转染后的HT-29细胞ATP水平上调,且转染后的HT-29侵袭能力增强。结论:研究结果提示ZAG可能通过调节ATP水平增强大肠癌HT-29细胞的侵袭能力,为大肠癌治疗提供了有价值的新靶点。Objective:Zinc-alpha-2-glycoprotein 1(ZAG) is a protein with multiple functions,such as participating in lipometabolism,saccharometabolism,energy metabolism,immunoreaction and fertilization. It is observed whether ZAG involved in the regulation of human colorectal cancer cell line(HT-29) in this study. Methods:ZAG-RNAi plasmids were constructed and transfected into human colorectal cancer HT-29 cells. The expressions of target proteins and gene were detected by Western blot and RT-PCR,respectively. Adenosine triphosphate(ATP) was assessed to investigate the activation of energy metabolism. The capacity of HT-29 cell migration was investigated using the Transwell migration assay. Results:ZAG interference plasmids were successfully transfected into HT-29 cells,and stably transfected cell lines were screened out. ATP level and the migration of ZAG inhibitor-treated cells were increased. Conclusion:The down-expression of ZAG promoted the expression of ATP and up-regulated the malignant phenotype ofHT-29 cells.
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