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    张小红, 李梦, 王超群, 巩玉森. 长链非编码RNA HOTAIR调控乳腺癌细胞放疗敏感性的研究[J]. 徐州医科大学学报, 2021, 41(4): 247-251. DOI: 10.3969/j.issn.2096-3882.2021.04.003
    引用本文: 张小红, 李梦, 王超群, 巩玉森. 长链非编码RNA HOTAIR调控乳腺癌细胞放疗敏感性的研究[J]. 徐州医科大学学报, 2021, 41(4): 247-251. DOI: 10.3969/j.issn.2096-3882.2021.04.003
    Long non-coding RNA HOTAIR regulates the radiosensitivity of breast cancer cells[J]. Journal of Xuzhou Medical University, 2021, 41(4): 247-251. DOI: 10.3969/j.issn.2096-3882.2021.04.003
    Citation: Long non-coding RNA HOTAIR regulates the radiosensitivity of breast cancer cells[J]. Journal of Xuzhou Medical University, 2021, 41(4): 247-251. DOI: 10.3969/j.issn.2096-3882.2021.04.003

    长链非编码RNA HOTAIR调控乳腺癌细胞放疗敏感性的研究

    Long non-coding RNA HOTAIR regulates the radiosensitivity of breast cancer cells

    • 摘要: 目的探讨长链非编码RNA (LncRNA) HOTAIR对乳腺癌细胞放疗敏感性的影响及其机制。方法检测乳腺癌组织、癌旁组织及常用乳腺癌细胞株中HOTAIR的表达情况,选取HOTAIR表达较低的SKBR3细胞株作为研究对象。通过慢病毒转染构建过表达HOTAIR乳腺癌细胞株。经放疗后,采用CCK-8实验、Transwell小室实验检测过表达HOTAIR乳腺癌细胞放疗前后的增殖和侵袭能力的变化情况。采用Western blot 技术检测HOTAIR对自噬信号通路中Beclin1、LC3Ⅰ、LC3Ⅱ和mTOR、p-mTOR等蛋白表达的影响。结果乳腺癌组织中的HOTAIR表达高于癌旁组织(P<0.05)。与人正常乳腺上皮细胞相比,LncRNA HOTAIR高表达于乳腺癌细胞株中(P<0.05)。HOTAIR过表达显著提高乳腺癌SKBR3细胞株的增殖和侵袭能力(P<0.05)。HOTAIR过表达组与阴性对照组相比,LC3Ⅱ/LC3Ⅰ比值和Beclin1蛋白的表达量增加,p-AKT和mTOR的表达水平降低(P<0.05);用mTOR受体抑制剂RAPA处理2组细胞放疗后发现,2组细胞mTOR蛋白和p-AKT蛋白的表达量均受到显著抑制,Beclin1蛋白的表达量和LC3Ⅱ/LC3Ⅰ比值均显著增高,但2组细胞间各蛋白表达无明显差异(P>0.05)。结论HOTAIR过表达提高了放疗后乳腺癌SKBR3细胞株的活力及侵袭能力,HOTAIR过表达能增强乳腺癌SKBR3细胞放射抵抗性。其机制可能与通过调控mTOR信号通路增强乳腺癌细胞自噬水平有关。

       

      Abstract: ObjectiveTo explore the effects of long non-coding RNA HOX transcript antisense intergenic RNA (HOTAIR) on radiotherapy sensitivity of breast cancer cells and related mechanism. MethodsThe expression of HOTAIR in breast cancer tissues and cell lines was detected. SKBR3 cell line with low HOTAIR expression was adopted in the following studies. Lentivirus transfection was used to establish the cells with overexpression of HOTAIR. After radiotherapy, their proliferation, viability and invasion were detected by plate colony formation assay, CCK-8 assay and Transwell chamber assay. The effects of HOTAIR on the expression of Beclin1, LC3Ⅰ, LC3Ⅱ, mTOR and p-mTOR were detected by Western blot.ResultsThe expression of HOTAIR in breast cancer tissues was higher than that in adjacent non-caner tissues (P<0.05). Compared with normal breast epithelial cells, lncRNA HOTAIR was highly expressed in breast cancer cell lines (P<0.05). The overexpression of HOTAIR significantly increased the proliferation, viability and invasion abilities of SKBR3 cells (P<0.05). Compared with the control group, the HOTAIR overexpression group presented increases in LC3Ⅱ/LC3Ⅰratio and Beclin1 expression as well as decreases in the expression of p-AKT and mTOR (P<0.05). After treatment with mTOR receptor inhibitor RAPA, the expression of mTOR and p-AKT was significantly inhibited in both groups, and the level of Beclin1 and LC3Ⅱ/LC3Ⅰratio significantly increased. There was no significant difference in the expression of the above proteins between the two groups (P>0.05). ConclusionsHOTAIR overexpression enhances the viability and invasion ability of SKBR3 cells after radiotherapy, as well as the radiation resistance of SKBR3 cells, which may be related to enhanced autophagy in breast cancer cells through regulation of the mTOR signaling pathway.

       

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