海兔素对人乳腺癌SK-BR-3细胞的抑制作用及机制研究

本文阐述了海兔素(Aplysin)对人乳腺癌SK-BR-3细胞增殖和凋亡的影响,并探讨了其可能的作用机制.分别采用CCK-8法和流式细胞术Annexin V-FITC/PI双染法测定不同剂量海兔素对SK-BR-3细胞的增殖抑制和凋亡诱导作用,并以Western blot测定SK-BR-3细胞中EGFR、Akt及ERK表达水平和磷酸化水平.结果发现,20、30、40、45、50、55、60 mg/L海兔素处理SK-BR-3细胞24 h后,细胞的生长增殖明显受到抑制,呈量效依赖性,其IC25和IC50值为分别为29.4和33.7 mg/L; IC25和IC50剂量海兔素可明显诱导细胞凋亡,并下调SK-BR-3细胞EGFR、Akt及ERK的磷酸化蛋白表达水平,但是不影响总蛋白表达水平.表明海兔素对人乳腺癌SK-BR-3细胞具有抑制增殖和诱导凋亡的作用,其作用机制可能与海兔素抑制细胞中EGFR蛋白磷酸化,进而阻断下游效应分子Akt和ERK的活化有关.

Effect of Aplysin on the Proliferation and Apoptosis in Human Breast Cancer SK-BR-3

The effects of aplysin,nature extract from Laurencia,on the proliferation and apoptosis on human breast cancer SK-BR-3 cells were investigated in this study.After treatment with aplysin at a serial of concentrations,cell proliferation was investigated by using Cell Counting Kit-8 and apoptosis was analyzed by Annexin V-FITC/PI staining via flow cytometry.The total and phosphorylated proteins of EGFR,Akt,and ERK were detected by western blot.The results showed that aplysin was able to inhibit SK-BR-3 cell proliferation in a concentration dependent manner within the concentration range of 20,30,40,45,50,55,and 60 mg/L.Aplysin could induce significant apoptosis at the dose of IC25 and IC50.Phosphorylation levels of the receptor of EGFR and cytoplasmic protein of Akt and ERK were significantly down-regulated by aplysin at the dose of IC25 and IC50,while their total protein expression levels were not affected.The results indicated that aplysin could inhibit SK-BR-3 cell proliferation and induce apoptosis by blocking EGFR/Akt and EGFR/ERK signal pathways.