| 宗斌,房栋,张文琪,刘意.沉默lncRNA-UCA1对乏氧诱导NSCLC细胞A549放射抵抗的作用机制.[J].中南医学科学杂志.,2023,(3):368-372. |
| 沉默lncRNA-UCA1对乏氧诱导NSCLC细胞A549放射抵抗的作用机制 |
| The mechanism of silencing lncRNA UCA1 on hypoxia induced radiation resistance in NSCLC cell line A549 |
| 投稿时间：2022-07-19 修订日期：2023-03-28 |
| DOI：10.15972/j.cnki.43-1509/r.2023.03.012 |
| 中文关键词: lncRNA-UCA1 乏氧 NSCLC 放射抵抗 Akt/mTOR通路 [ |
| 英文关键词:lncRNA-UCA1 hypoxia A549 cell radiation resistance Akt/mTOR pathway |
| 基金项目:江苏省科学研究与发展计划(2020039412-16) |
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| 中文摘要: |
| 目的探究沉默长链非编码RNA尿路上皮癌相关基因1(lncRNA-UCA1)对乏氧诱导的非小细胞肺癌(NSCLC)细胞A549放射抵抗的作用机制。 方法选取NSCLC细胞A549及人正常支气管上皮细胞HBE,平板克隆实验、qRT-PCR分别检测不同NSCLC细胞在常氧和乏氧状态下对放射的敏感性及lncRNA-UCA1的表达水平。将A549细胞实验分为si-NC组(未干预)及si-RNA组(转染lncRNA-UCA1)。流式细胞术检测乏氧状态下两组细胞放射敏感性、细胞分期和凋亡率。裸鼠成瘤实验检测乏氧状态下两组裸鼠成瘤能力。Western blotting检测两组B细胞淋巴瘤-2(Bcl-2)、Bcl-2相关X蛋白(BAX)、磷酸化蛋白质丝氨酸苏氨酸激酶(p-Akt)及磷酸化雷帕霉素靶蛋白(p-mTOR)含量。 结果A549细胞放射敏感性显著高于HBE；乏氧状态下A549细胞lncRNA-UCA1表达水平显著高于常氧状态。沉默lncRNA-UCA1可以逆转放射诱导的周期阻滞,诱导细胞凋亡。与si-NC组比较,si-RNA组肿瘤增殖变慢,肿瘤体积变小,p-Akt、p-mTOR和Bcl-2蛋白含量显著下调,BAX蛋白含量显著上调。 结论沉默lncRNA-UCA1能激活Akt/mTOR通路抑制NSCLC A549细胞的放射抵抗,增加其放射治疗敏感性。 |
| 英文摘要: |
| AimTo investigate the mechanism of silencing long chain non-coding RNA urothelial cancinoma associated gene 1 (lncRNA-UCA1) on hypoxia induced radiation resistance of non-small cell lung cancer (NSCLC) cell line A549. MethodsNSCLC cell A549 and human normal bronchial epithelial cell HBE were selected, and plate cloning experiments and qRT-PCR were performed to detect the radiosensitivity of different NSCLC cells under normoxic and hypoxic conditions, as well as the expression level of lncRNA UCA1. A549 cell experiments were divided into si-NC group (without intervention) and si-RNA group (transfected with lncRNA UCA1). Flow cytometry was used to detect the radiosensitivity, cell stage, and apoptosis rate of the two groups under hypoxic conditions. The nude mouse tumor formation experiment detected the tumor formation ability of two groups of nude mice under hypoxic conditions. Western blotting was used to detect the expression of B cell lymphomatoma 2 (Bcl-2), Bcl-2 associated X (BAX), phosphorylated protein serine threonine kinase (p-Akt), and phosphorylated rapamycin target protein (p-mTOR) in two groups. ResultsThe radiosensitivity of A549 cells was significantly higher than that of HBE; The expression level of lncRNA UCA1 in A549 cells under hypoxic conditions was significantly higher than that under normoxic conditions. Silencing lncRNA-UCA1 can reverse radiation induced cycle arrest and induce cell apoptosis. Compared with the si-NC group, the si-RNA group showed slower tumor proliferation, smaller tumor volume, significantly downregulation of p-Akt, p-mTOR, and Bcl-2 protein expression levels, and significantly upregulation of BAX protein expression levels. ConclusionSilencing lncRNA UCA1 activates the Akt/mTOR pathway to inhibit the radiation resistance of NSCLC A549 cells and increase their sensitivity to radiation therapy. |
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