中文摘要：

目的：研究mi R-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 Gyγ射线连续照射宫颈癌Hela、Siha细胞诱导辐射抗性细胞株;采用micro RNA芯片技术比较辐射抗性细胞与亲本细胞中mi RNA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mi R-1290的表达水平;借助mi R-1290及mi R-1290-inhibition慢病毒表达载体,调变mi R-1290在Hela细胞的表达;调变mi R-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mi R-1290表达水平显著升高（P〈0.05）;乏氧和辐射可诱导mi R-1290在宫颈癌Hela细胞中表达（P〈0.05）;上调表达mi R-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mi R-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mi R-1290在宫颈癌Hela细胞中表达,mi R-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 mi R-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 γ-ray. The differential expression patterns of mi RNAs between radioresistant cells and parental cells were evaluated using mi RNA microarray. The expression level of mi R-1290 was detected in Hela cells treated under different conditions of hypoxia and radiation. The lentivirus of mi R-1290 and mi R-1290-inhibition were used to modulate the expression of mi R-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 mi R-1290. Western Blot was used to detect the expression level of E-cadherin and N-cadherin. Results： Mi R-1290 expression were significantly upregulated in radioresistant cervical cancer cells（P〈0.05）. The radiation and hypoxia induced the expression of mi R-1290 in cervical cancer Hela cells（P〈0.05）. Up-regulating the expression of mi R-1290 enhanced abilities of migration and invasion of Hela cells and Hela cells presented the mesenchymal cell phenotypes（P〈0.05）. The mi R-1290 overexpression decreased the expression of E-cadherin and increased the expression of N-cadherin in Hela cells（P〈0.05）. Conclusions： These results demonstrated that hypoxia and radiation up-regulated the expression of mi R-1290 in cervical cancer Hela cells and mi R-1290 promoted the EMT of Hela cells by modulating the expression of E-cadherin and N-cadherin.