Abstract：
BACKGROUND: NOP58 ribonucleoprotein (NOP58) is associated with the recurrence of lung adenocarcinoma.
OBJECTIVE: Few investigations concentrate on the role of NOP58 in non-small cell lung cancer (NSCLC), which is the focus of our current study.
METHODS: Following transfection, the proliferation, migration, and invasion of NSCLC cells were assessed by 5- ethynyl-2\'-deoxyuridine (EdU), wound healing, and transwell assays. The percentage of CD9+ cells was evaluated by flow cytometry assay. Based on target genes and binding sites predicted through bioinformatics analysis, a dual-luciferase reporter assay was performed to verify the targeting relationship between hsa_circ_0001550 and NOP58. The effect of NOP58 overexpression on hsa_circ_0001550 stability was gauged using Actinomycin D. The hsa_circ_0001550 and NOP58 expression levels, as well as protein expressions of CD44, CD133, OCT4, and SOX2 in NSCLC cells were determined by quantitative real-time PCR and Western blot, respectively.
RESULTS: Hsa_circ_0001550 was remarkably up-regulated in NSCLC cell lines A549 and PC9, silencing of which weakened cell abilities to proliferate, migrate and invade, decreased CD9+ cell ratio, and diminished protein expressions of CD44, CD133, OCT4, and SOX2. NOP58 could bind to hsa_circ_0001550 and stabilize its expression, and NOP58 overexpression partially abrogated hsa_circ_0001550 knockdown-inhibited NSCLC cell proliferation, migration, invasion and stemness.
CONCLUSIONS: Overexpression of NOP58 facilitates proliferation, migration, invasion, and stemness of NSCLC cells by stabilizing hsa_circ_0001550, hinting that NOP58 is a novel molecular target for NSCLC therapy.
OBJECTIVE: Few investigations concentrate on the role of NOP58 in non-small cell lung cancer (NSCLC), which is the focus of our current study.
METHODS: Following transfection, the proliferation, migration, and invasion of NSCLC cells were assessed by 5- ethynyl-2\'-deoxyuridine (EdU), wound healing, and transwell assays. The percentage of CD9+ cells was evaluated by flow cytometry assay. Based on target genes and binding sites predicted through bioinformatics analysis, a dual-luciferase reporter assay was performed to verify the targeting relationship between hsa_circ_0001550 and NOP58. The effect of NOP58 overexpression on hsa_circ_0001550 stability was gauged using Actinomycin D. The hsa_circ_0001550 and NOP58 expression levels, as well as protein expressions of CD44, CD133, OCT4, and SOX2 in NSCLC cells were determined by quantitative real-time PCR and Western blot, respectively.
RESULTS: Hsa_circ_0001550 was remarkably up-regulated in NSCLC cell lines A549 and PC9, silencing of which weakened cell abilities to proliferate, migrate and invade, decreased CD9+ cell ratio, and diminished protein expressions of CD44, CD133, OCT4, and SOX2. NOP58 could bind to hsa_circ_0001550 and stabilize its expression, and NOP58 overexpression partially abrogated hsa_circ_0001550 knockdown-inhibited NSCLC cell proliferation, migration, invasion and stemness.
CONCLUSIONS: Overexpression of NOP58 facilitates proliferation, migration, invasion, and stemness of NSCLC cells by stabilizing hsa_circ_0001550, hinting that NOP58 is a novel molecular target for NSCLC therapy.
摘要：
背景：NOP58核糖核蛋白（NOP58）与肺腺癌的复发有关。
目的：很少有研究关注NOP58在非小细胞肺癌（NSCLC）中的作用，这是我们当前研究的重点。
方法：转染后，扩散,迁移,NSCLC细胞的侵袭性通过5-乙炔基-2'-脱氧尿苷（EdU）评估，伤口愈合，和transwell分析。通过流式细胞术测定评估CD9+细胞的百分比。基于通过生物信息学分析预测的靶基因和结合位点，进行双荧光素酶报告基因测定以验证hsa_circ_0001550和NOP58之间的靶向关系。用放线菌素D测定NOP58过表达对hsa_circ_0001550稳定性的影响。实时定量PCR和Westernblot检测NSCLC细胞中CD44、CD133、OCT4和SOX2的蛋白表达,分别。
结果：Hsa_circ_0001550在NSCLC细胞系A549和PC9中显著上调，沉默后细胞增殖能力减弱，迁移和入侵，CD9+细胞比例降低，CD44、CD133、OCT4和SOX2的蛋白表达减少。NOP58可以与hsa_circ_0001550结合并稳定其表达，和NOP58过表达部分消除hsa_circ_0001550敲低抑制NSCLC细胞增殖，迁移,入侵和干。
结论：NOP58过表达促进增殖，迁移,入侵,通过稳定hsa_circ_0001550来提高NSCLC细胞的干性，暗示NOP58是NSCLC治疗的新分子靶标。
目的：很少有研究关注NOP58在非小细胞肺癌（NSCLC）中的作用，这是我们当前研究的重点。
方法：转染后，扩散,迁移,NSCLC细胞的侵袭性通过5-乙炔基-2'-脱氧尿苷（EdU）评估，伤口愈合，和transwell分析。通过流式细胞术测定评估CD9+细胞的百分比。基于通过生物信息学分析预测的靶基因和结合位点，进行双荧光素酶报告基因测定以验证hsa_circ_0001550和NOP58之间的靶向关系。用放线菌素D测定NOP58过表达对hsa_circ_0001550稳定性的影响。实时定量PCR和Westernblot检测NSCLC细胞中CD44、CD133、OCT4和SOX2的蛋白表达,分别。
结果：Hsa_circ_0001550在NSCLC细胞系A549和PC9中显著上调，沉默后细胞增殖能力减弱，迁移和入侵，CD9+细胞比例降低，CD44、CD133、OCT4和SOX2的蛋白表达减少。NOP58可以与hsa_circ_0001550结合并稳定其表达，和NOP58过表达部分消除hsa_circ_0001550敲低抑制NSCLC细胞增殖，迁移,入侵和干。
结论：NOP58过表达促进增殖，迁移,入侵,通过稳定hsa_circ_0001550来提高NSCLC细胞的干性，暗示NOP58是NSCLC治疗的新分子靶标。
