UNASSIGNED: NSCLC cell-based cultures including A549 and H460 were employed for such an investigation. hsa_circ_0003489, miR-98-5p, and insulin-like growth factor 2 (IGF2) expression-profiles were evaluated with a quantitative real-time polymerase chain reaction (RT-qPCR). The PTX resistance was determined using MTT assay, and the ELISA test measured IGF2 expression. Facilitating corroboration for miR-98-5p relation and hsa_circ_0003489 or IGF2, a dual-luciferase reporter method was applied.
UNASSIGNED: The hsa_circ_0003489 level was raised in cells and tissues from PTX-resistant (PR) NSCLC. In PR NSCLC cells, hsa_circ_0003489 knockdown reduced PTX resistance. For the purpose of the mechanism study, hsa_circ_0003489 knockdown substantially reduced IGF2 expression via miR-98-5p sponging, improving PTX sensitivity in PR NSCLC.
UNASSIGNED: Through miR-98-5p/IGF2 axis control, hsa_circ_0003489 knockdown helped NSCLC overcome PTX resistance, suggesting a potential circRNA-targeted therapy for the disease.
包括A549和H460的基于NSCLC细胞的培养物用于这样的研究。hsa_circ_0003489,miR-98-5p,用定量实时聚合酶链反应(RT-qPCR)评估胰岛素样生长因子2(IGF2)的表达谱。使用MTT测定法测定PTX抗性,和ELISA测试测量IGF2表达。促进miR-98-5p关系和hsa_circ_0003489或IGF2的确证,应用双荧光素酶报告方法。
■来自PTX抗性(PR)NSCLC的细胞和组织中的hsa_circ_0003489水平升高。在PRNSCLC细胞中,hsa_circ_0003489敲低降低了PTX抗性。出于机理研究的目的,hsa_circ_0003489敲低通过miR-98-5p海绵作用显著降低IGF2表达,改善PTX在PR非小细胞肺癌中的敏感性。
■通过miR-98-5p/IGF2轴控制,hsa_circ_0003489敲除帮助非小细胞肺癌克服PTX耐药,提示该疾病的潜在circRNA靶向治疗。