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机构地区:[1]重庆医科大学基础医学院病理学教研室,重庆400016
出 处:《第三军医大学学报》2008年第3期237-240,共4页Journal of Third Military Medical University
基 金:重庆市自然科学基金(2006BB52881)~~
摘 要:目的探讨多聚(腺苷二磷酸核糖)聚合酶[Poly(ADP-ribose)polymerases,PARPs]抑制剂5-氨基异喹啉酮[5-Aminoisoquinolinone.HCl,5-AIQ]对小鼠结肠腺癌CT26细胞基质黏附、运动、侵袭能力的影响。方法应用Westernblot检测5-AIQ对PARP表达的影响,细胞-基质黏附实验、细胞运动及侵袭实验观察5-AIQ抑制CT26细胞PARP后,其基质黏附、运动及侵袭能力的变化。结果5-AIQ处理组PARP表达明显弱于未处理组(P<0.05);黏附实验结果显示,与5-AIQ未处理组比较,5-AIQ100、500μmol/L处理组的吸光度值明显降低(P<0.01),其黏附抑制率分别是14.54%、21.69%;运动及侵袭实验中,5-AIQ500μmol/L处理组与未处理组的细胞数差别显著(P<0.05),其运动及侵袭抑制率分别是30.09%、37.47%。结论5-AIQ可抑制CT26细胞PARP的表达,并可降低CT26细胞基质黏附、运动及侵袭能力,5-AIQ在抗肿瘤侵袭转移中可能发挥作用。Objective To study the effect of poly(ADP-ribose) polymerase (PARP) inhibitor 5-AIQ on the adhesion, migration and invasion of mouse colon adenocarcinoma cell line (CT26). Methods The expres- sion of PARP after 5-AIQ treatment was detected Western blot. The cell adhesion, migration and invasion of CT26 after 5-AIQ treatment were observed by cell-matrix adhesion assay, cell migration assay and matrigel invasion assay. Results The expression of PARP in 5-AIQ-treated CT26 was weaker than that in 5-AIQ-untreated cells (P 〈 0.05). In the adhesion assay, the OD value of 5-AIQ-treated cells was reduced as compared with untreated cells (P 〈0.05) and the inhibition rate of 100 μmol/L 5-AIQ treated cells and 500 μmol/L 5-AIQ treated cells was 14.54% and 21.69% respectively. Moreover, migration and invasion potential of CT26 were also reduced by 500 μmol/L 5-AIQ treatment (P 〈0.05), and the inhibition rate was 30.09% and 37.47% for migration and invasion respectively. Conclusion PARP inhibitor 5-AIQ can reduce the expression of PARP, adhesion, migration and invasion of CT26 ceils, suggesting 5-AIQ probably plays a role against tumor metastasis.
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