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首页> 外文期刊>RSC Advances >Long noncoding RNA ANRIL knockdown increases sensitivity of non-small cell lung cancer to cisplatin by regulating the miR-656-3p/SOX4 axis
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Long noncoding RNA ANRIL knockdown increases sensitivity of non-small cell lung cancer to cisplatin by regulating the miR-656-3p/SOX4 axis

机译：通过调节miR-656-3P / SOX4轴，长度非划分RNA anril敲低增加了非小细胞肺癌对顺铂的敏感性

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Long noncoding RNAs (lncRNAs) are implicated in the development of chemoresistance in many cancers. However, the effect and mechanism of lncRNA antisense noncoding RNA in the INK4 locus (ANRIL) on cisplatin (CDDP) resistance in non-small cell lung cancer (NSCLC) remain unclear. The levels of ANRIL, microRNA (miR)-656-3p and sex-determining region Y-related high-mobility group box 4 (SOX4) in NSCLC tissues and cells were detected by quantitative real-time polymerase chain reaction or western blotting. Cell viability, apoptosis, migration and epithelial-to-mesenchymal transition (EMT) were assessed by using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide (MTT assay), flow cytometry, trans-well assays and western blotting, respectively. The xenograft model was established using CDDP-resistant NSCLC cells. The target association between miR-656-3p and ANRIL or SOX4 was validated by luciferase reporter assay and RNA immunoprecipitation. ANRIL expression was increased in CDDP-resistant NSCLC tissues and cells. Knockdown of ANRIL decreased cell viability, migration and EMT but induced apoptosis in CDDP-resistant NSCLC cells. Moreover, silencing of ANRIL reduced xenograft tumor growth in vivo . miR-656-3p was targeted by ANRIL and its exhaustion attenuated the suppressive role of ANRIL knockdown in CDDP resistance in NSCLC cells. SOX4 acted as a target of miR-656-3p and was positively regulated by ANRIL. Collectively, interference of ANRIL repressed CDDP resistance through promoting apoptosis and inhibiting cell viability, migration and EMT by up-regulating miR-656-3p and down-regulating SOX4, indicating a new target to improve the chemotherapeutic efficacy in NSCLC.
机译：长期非编码RNA（LNCRNA）涉及在许多癌症中的化学抑制的发展中。然而，在非小细胞肺癌（NSCLC）中的Ink4基因座（AnRIL）中LNCRNA反义Noncoding RNA的效果和机制仍然尚不清楚。通过定量的实时聚合酶链反应或蛋白质印迹检测NSCLC组织和细胞中的anril，microRNA（miR）-656-3p和性测定区域Y相关型高迁移率组箱4（SOx4）。通过使用3-（4,5-二甲基噻唑-2-基）-2,5-二苯基 - 四唑溴（MTT测定），流式细胞仪评估细胞活力，细胞凋亡，迁移和上皮对间充质转换（EMT），流式细胞仪评估微井测定和蛋白质印迹。使用CDDP抗性NSCLC细胞建立异种移植模型。通过Luciferase报道和RNA免疫沉淀验证MIR-656-3P和ANRIL或SOX4之间的靶关节。在CDDP抗性NMSCLC组织和细胞中增加了anril表达。 anril的敲低降低细胞活力，迁移和EMT，但诱导CDDP抗性NSCLC细胞的细胞凋亡。此外，anril的沉默降低了体内异种移植肿瘤生长。 miR-656-3p是由anril的靶向，其耗尽衰减了anril敲低在Nsclc细胞中CDDP抗性的抑制作用。 SOX4充当miR-656-3p的靶标，受到anril的正规调节。通过促进细胞凋亡和抑制细胞活力，迁移和EMT来集体，通过促进miR-656-3p和下调SOx4，表明新的靶标以提高NSCLC中的化学治疗效果的新靶标，通过促进细胞凋亡和抑制细胞活力，迁移和EMT。

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