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首页> 外文期刊>Thoracic cancer. >miRNA‐218‐5p increases cell sensitivity by inhibiting PRKDC activity in radiation‐resistant lung carcinoma cells
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miRNA‐218‐5p increases cell sensitivity by inhibiting PRKDC activity in radiation‐resistant lung carcinoma cells

机译：MiRNA-218-5P通过抑制抗抗肺癌细胞中的PRKDC活性来增加细胞敏感性

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Background Non‐small cell lung carcinoma (NSCLC) is a malignancy with the highest mortality rate. Currently, surgery combined with radiotherapy is the first choice in the clinical treatment of lung carcinoma (LC); however, long‐term radiotherapy leads to radiation resistance in patients, resulting in treatment failure. Methods In this study, a new microRNA‐218‐5p (miRNA‐218‐5p) was identified, and its function in LC was investigated. Results Reverse transcription quantitative polymerase chain reaction (RT‐qPCR) results revealed that miRNA‐218‐5p was downregulated in LC. Overexpression or inhibition of miRNA‐218‐5p in LC and targeted binding of protein kinase, DNA‐activated, catalytic polypeptide (PRKDC) to miRNA‐218‐5p were confirmed by comprehensive bioinformatic analysis. Exosomes from A549 and H1299 cells were cocultured with miRNA‐218‐5p and then cotransfected into radiation‐resistant A549R and H1299R cells; the proliferation of radiation‐resistant LC cells was found to be effectively inhibited and apoptosis was induced. Overexpression of miRNA‐218‐5p and X‐irradiation could enhance the radiosensitivity of LC cells. Exogenous miRNA‐218‐5p derived from A549 and H1299 cells could be transfected into radiation‐resistant LC cells and could inhibit PRKDC expression, thus accelerating DNA damage, apoptosis, and radiation sensitization of LC cells. Conclusions miRNA‐218‐5p could induce apoptosis and enhance the radiosensitivity of LC cells through regulatory activities, thus suggesting its application as a potential target for LC treatment.
机译：背景技术非小细胞肺癌（NSCLC）是具有最高死亡率的恶性肿瘤。目前，手术结合放疗是肺癌（LC）临床治疗的首选;然而，长期放疗导致患者的抗辐射抗性导致治疗失败。方法在本研究中，鉴定了新的MicroRNA-218-5P（miRNA-218-5p），并研究了其在LC的功能。结果逆转录定量聚合酶链反应（RT-QPCR）结果显示，MiRNA-218-5P在LC下调。通过综合生物信息分析证实了通过综合生物信息分析证实了LC蛋白激酶，DNA活化的，催化多肽（PRKDC）至miRNA-218-5P的靶向蛋白激酶的靶向结合的过表达或抑制作用。来自A549和H1299细胞的外泌体与miRNA-218-5P共培养，然后通过COTANSFECTOCTE耐抗辐射A549R和H1299R细胞。发现抗辐射LC细胞的增殖被发现有效抑制，诱导细胞凋亡。 MiRNA-218-5P和X辐射的过表达可以增强LC细胞的放射敏感性。可以将来自A549和H1299细胞衍生自A549和H1299细胞的外源miRNA-218-5P转染到抗辐射的LC细胞中，并且可以抑制PRKDC表达，从而加速LC细胞的DNA损伤，细胞凋亡和辐射敏化。结论MiRNA-218-5P可以诱导细胞凋亡并通过调节活动提高LC细胞的放射敏感性，从而提示其作为LC治疗潜在目标的应用。

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