| 马 越,张凤春,王红霞.RAd-p53、E1B--OLV及紫杉醇对乳腺癌干细胞的作用[J].中国肿瘤,2013,22(7):575-580. |
| RAd-p53、E1B--OLV及紫杉醇对乳腺癌干细胞的作用 |
| Role of RAd-p53、E1B--OLV and Paclitaxel on Breast Cancer Stem Cells |
| 投稿时间：2012-10-05 |
| DOI：10.11735/j.issn.1004-0242.2013.07.A013 |
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| 中文关键词: 溶瘤病毒 化疗 乳腺癌干细胞 微球体 CD44+CD24-细胞 |
| 英文关键词:oncolytic virus chemotherapy breast cancer stem cells mammosphere CD44+CD24- cell |
| 基金项目: |
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| 摘要点击次数: 1959 |
| 全文下载次数: 719 |
| 中文摘要: |
| 摘 要：［目的］ 研究重组p53腺病毒(RAd-p53)、E1B蛋白缺陷型溶瘤腺病毒(E1B--OLV)及化疗药物紫杉醇对乳腺癌干细胞的作用。［方法］分别用RAd-p53、E1B--OLV、紫杉醇感染人乳腺癌细胞系MCF-7细胞，并常规培养MCF-7细胞。流式细胞仪(FCM)分析CD44+CD24-细胞的表型比例，及行微球体培养，观察微球体大小，用FCM分析微球体CD44+CD24-细胞的比例。［结果］ RAd-p53感染MCF-7细胞的CD24-，CD44+，CD44+CD24-比例为（3.670±0.577）%，（53.300±0.580）%，（0.930±0.116）%(P<0.05)；E1B--OLV感染组为（24±1）%，（60±1）%，（10.670±1.528）% (P<0.05)；紫杉醇组为（14±1）%，（3.670±0.577）%，（2.330±1.528）%(P>0.05)，对照组为（14±1）%，（50±1）%，（2.270±0.643）%。RAd-p53感染组及E1B--OLV感染组的微球体大小与对照组相仿，成球时间早于对照组，紫杉醇组的微球体小于对照组，成球时间则晚于对照组。RAd-p53组微球体中CD24-，CD44+，CD44+CD24- 的比例为（3.670±0.577）%，（44.670±0.577）% ，（17±1）%(P<0.05)；E1B--OLV组为（24.670±0.577）%，（29.670±1.528）%，（23.5±0.5）% (P<0.05)；紫杉醇组为（77.330±1.528）%，（1.100±0.361）% (P<0.05)，（19±1）% (P>0.05)；对照组为（11±1）%，（50±1）%，（20.330±1.528）%。［结论］ RAd-p53促进BCSCs分化成增殖祖细胞，减少了CD44+CD24- 细胞比例。E1B--OLV病毒杀伤MCF-7细胞，加快BCSCs自我更新，促进其分化成干细胞性质的子代。紫杉醇能杀死MCF-7细胞，对BCSCs无杀伤或促进其分化作用。 |
| 英文摘要: |
| Abstract:［Purpose］ To investigate the role of recombinant Ad-p53(RAd-p53)，E1B protein-dificient oncolytic adenovirus (E1B--OLV) and chemotherapeutic agent paclitaxel on breast cancer stem cells (BCSCs).［Methods］ The human breast cancer cell line MCF-7 was infected by RAd-p53，E1B--OLV and paclitaxel. The MCF-7 cells were cultured routinely. The proportion of CD44+CD24- cells were assessed by flow cytometry(FCM) in four groups respectively. Meanwhile，mammosphere was cultured in four groups’ cells to observe the sizes of mammospheres. The proportion of CD44+CD24- cells in four groups were assessed by FCM.［Results］ Proportion of CD24-，CD44+，CD44+CD24- in MCF-7 cells infected by RAd-p53 was(3.670±0.577)%，(53.300±0.580)%，(0.930±0.116)% (P<0.05). which was(24±1)%，(60±1)%，(10.670±1.528)%(P<0.05) in the E1B--OLV group. In the paclitaxel group，the proportion was(14±1)%，(3.670±0.577)%，(2.330±1.528)%(P>0.05). Meanwhile，in the control group，the proportion was(14±1)%，(50±1)%，(2.270±0.643)%. In the RAd-p53 and E1B--OLV groups，the time of mammosphere’s formation was earlier than that in control group，the volumes were equal to control group. In the paclitaxel group，the time of mammosphere’s formation was later，the volume was smaller than control group. The proportion of CD24-，CD44+，CD44+CD24- in the RAd-p53 group was(3.670±0.577)%，(44.670±0.577)%，(17±1)%(P<0.05)，In the E1B--OLV group，the proportion was(24.670±0.577)%，(29.670±1.528)%，(23.5±0.5)% (P<0.05). In the paclitaxel group，the proportion were (77.330±1.528)%，(1.100±0.361)%(P<0.05)，(19±1)%(P>0.05). Meanwhile，in the control group，the proportion was(11±1)%，(50±1)%，(20.330±1.528)%.［Conclusion］ RAd-p53 accelerates the speed of BCSCs differentiation to progenitor cells and decreases the proportion of CD44+CD24- cells. E1B--OLV kills MCF-7 cells. It also accelerates the speed of self-renewed and differentiation of the BCSCs into the progeny of stem cell-like properties. Paclitaxel kills MCF-7 cells but have little effect on BCSCs. |
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