摘要
目的探讨PI-103对卵巢癌恶性表型的调控及其对卵巢癌脂肪酸合酶(FASN)表达的影响。方法 Western blot检测卵巢癌细胞株A2780,SKOV3/DDP和SKOV3中FASN的表达(对照组);将FASN表达量最高的细胞株A2780用药物PI-103处理(实验组)。采用MTT测定细胞抑制率、平板克隆形成实验和Transwell小室实验比较实验组与对照组的细胞生物学特性,Western blot比较两组细胞的FASN、p-Akt和p-rpS6表达。结果随着时间的延长,实验组的细胞增殖能力较对照组减弱(P<0.05)、克隆形成率降低[(8.45±1.04)%vs.(15.40±0.82)%](P<0.05)、侵袭细胞数减少[(58.67±6.51)个vs.(156.33±4.04)个](P<0.05)。实验组FASN、p-Akt和p-rpS6的蛋白表达水平均低于对照组(P<0.05)。结论 PI-103可有效抑制卵巢癌A2780细胞的PI3K/AKT/mTOR信号通路中相关蛋白的表达;在体外显著抑制细胞的增殖和侵袭。
Objective To explore the effect of PI-103 on ovarian malignant phenotype and fatty acid synthase（FASN） expression. Methods The expression of FASN in ovarian cancer cell lines A2780,SKOV3/DDP and SKOV3 was detected by Western blot（group B, as the control）, of which A2780 was with the highest expression level of FASN and treated with PI-103 （group A）. The biological characteristics detected by MTT, plate clone formation assay and Transwell assay were compared between two groups. The expressions of p-Akt, p-rpS6 and FASN proteins in the PI3K/ mTOR pathway were detected by Western blot and compared between two groups as well. Results Compared with A2780 cells in group B, as time went on, PI-103 significantly inhibited the growth of those in group A, with decreased viability, colon formation rate[（8. 45 ±1.04）% vs. （15. 40 ±0. 82）%] （P〈0.05）, and the number of cells travelling through the matrigel [（58. 67±6.51） pieces vs. （156. 33±4. 04） pieces]（P〈0. 05）. Compared with group B, PI-103 significantly down-regulated the expressions of p-Akt, p-rpS6 and FASN in group A（P〈0. 05）. Conclusion PI-103 significantly inhibits the PI3K/AKT/mTOR signaling pathway and effectively down-regulates relative protein expression and in vivo inhibits proliferation and invasion of ovarian cancer A2780 cells.
出处
《江苏医药》
CAS
北大核心
2014年第10期1123-1126,共4页
Jiangsu Medical Journal
