| 任正华 王艳飞 陈永斌 苗霞 任东青
王峰 郎海洋 郭娟 王晋 李予蓉 刘军叶.乏氧和辐射诱导的miR-1290 促进宫颈癌细胞EMT发生[J].,2016,16(17):3261-3267 |
| 乏氧和辐射诱导的miR-1290 促进宫颈癌细胞EMT发生 |
| Hypoxia and Radiation Induced miR-1290 Promotes the EMT of CervicalCancer Cell |
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| DOI： |
| 中文关键词: 辐射 乏氧 miR-1290 宫颈癌 上皮间质转化 |
| 英文关键词: Radiation Hypoxia MiR-1290 Cervical cancer EMT |
| 基金项目:国家自然科学基金项目（81272490；31470828） |
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| 中文摘要: |
| 目的：研究miR-1290 在宫颈癌Hela 细胞上皮间质转化中的作用。方法：模拟肿瘤放射治疗的分割疗法，单次2 Gy 酌射线连
续照射宫颈癌Hela、Siha细胞诱导辐射抗性细胞株；采用microRNA 芯片技术比较辐射抗性细胞与亲本细胞中miRNA的表达谱
差异；经不同条件乏氧和辐射处理宫颈癌Hela 细胞后检测miR-1290的表达水平；借助miR-1290 及miR-1290-inhibition慢病毒
表达载体，调变miR-1290 在Hela 细胞的表达；调变miR-1290后，划痕实验及Transwell 侵袭实验比较Hela 细胞的侵袭和转移能
力；蛋白质印迹法检测细胞中E 钙黏素(E-cadherin) 和N 钙黏素(N-cadherin) 的表达。结果：在宫颈癌辐射抗性细胞中miR-1290
表达水平显著升高(P<0.05)；乏氧和辐射可诱导miR-1290 在宫颈癌Hela 细胞中表达(P<0.05)；上调表达miR-1290，Hela 细胞出现
了明显的间质细胞的形态改变，细胞的侵袭和转移能力明显增强(P<0.05)。在Hela 细胞中上调表达miR-1290，降低了细胞中
E-cadherin 的表达，同时升高了N-cadherin 的表达(P<0.05)。结论：乏氧和辐射可诱导miR-1290 在宫颈癌Hela 细胞中表达，
miR-1290 通过调控E-cadherin 和N-cadherin 的表达促进宫颈癌Hela细胞发生EMT。 |
| 英文摘要: |
| Objective:To explore the role of miR-1290 in epithelial-mesenchymal transition of cervical cancer Hela cell.Methods:The radioresistant cervical cancer Hela cells and Siha cells were established by applying fractionated radiation consisted of a fraction
dose of around 2 Gy of 酌-ray. The differential expression patterns of miRNAs between radioresistant cells and parental cells were
evaluated using miRNA microarray. The expression level of miR-1290 was detected in Hela cells treated under different conditions of
hypoxia and radiation. The lentivirus of miR-1290 and miR-1290-inhibition were used to modulate the expression of miR-1290 in Hela
cells. The wound healing and Transwell were used to compare the abilities of migration and invasion of Hela cells with different
expression level of miR-1290. Western Blot was used to detect the expression level of E-cadherin and N-cadherin.Results:MiR-1290
expression were significantly upregulated in radioresistant cervical cancer cells (P<0.05). The radiation and hypoxia induced the
expression of miR-1290 in cervical cancer Hela cells (P<0.05). Up-regulating the expression of miR-1290 enhanced abilities of migration
and invasion of Hela cells and Hela cells presented the mesenchymal cell phenotypes (P<0.05). The miR-1290 overexpression decreased
the expression of E-cadherin and increased the expression of N-cadherin in Hela cells (P<0.05).Conclusion:These results demonstrated
that hypoxia and radiation up-regulated the expression of miR-1290 in cervical cancer Hela cells and miR-1290 promoted the EMT of
Hela cells by modulating the expression of E-cadherin and N-cadherin. |
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