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作 者:张寅 郑书荣[2] 张玮[2] 黄奇迪[2] 郭贵龙[2]
机构地区:[1]浙江省温州市第八人民医院普通外科,325000 [2]温州医学院附属第一医院肿瘤外科,325000
出 处:《实用医学杂志》2011年第24期4361-4363,共3页The Journal of Practical Medicine
基 金:浙江省卫生厅项目(编号:2009B106);温州市鹿城区科技局项目(编号:S080219)
摘 要:目的:探讨微小RNA 155(microRNA-155,miR-155)反义寡核苷酸(antisense oligonucleotide,ASO)对乳腺癌细胞增殖和凋亡的影响。方法:设计合成全硫代磷酸化修饰的miR-155 ASO,通过LipofectamineTM2000(Invitrogen)转染于乳腺癌HS578T细胞。CCK-8法检测乳腺癌细胞转染后的增殖情况,流式细胞仪分析转染率并检测细胞凋亡情况。结果:流式细胞仪检测转染率达70.5%。CCK-8试验结果显示转染miR-155 ASO后,HS578T细胞存活数明显低于空白组和脂质体组。流式细胞仪检测显示转染miR-155ASO后,HS578T细胞凋亡数明显增加。结论:miR-155 ASO可抑制乳腺癌HS578T细胞增殖,并促进其凋亡。提示miR-155可能成为乳腺癌治疗的靶基因。Objective To investigate the effects of antisense oligonucleotide (ASO) targeting miR-155 on the proliferation and apoptosis of HS578T cells. Methods Specific phosphorothioate antisense oligodeoxynucleotides targeting miR-155 was synthesized and then transfected into the breast cancer cells HS578T by Invitrogen's LipofectamineTM 2000. Cell counting kit-8 (CCK-8) assay was used to detect the proliferation of HS578T, transfection efficiency and cell apoptosis rate were detected by flow cytometry. Results Transfection efficiency detected by flow cytometry was 70.5%. CCK-8 assay showed that the viability of HS578T cells was reduced great]y after transfection with miR-155 ASO as compared with that in blank group or liposomes group. Transfection with miR-155 ASO could promote apoptosis greatly. Conclusions MiR-155 ASO could suppress the proliferation of HS578T and promote its apoptosis, which indicate that miR-155 may be a target gene for the treatment for breast carcinoma.
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