circHIPK3 Acts as Competing Endogenous RNA and Promotes Non-Small-Cell Lung Cancer Progression through the miR-107/BDNF Signaling Pathway.

circHIPK3 Acts as Competing Endogenous RNA and Promotes Non-Small-Cell Lung Cancer Progression through the miR-107/BDNF Signaling Pathway.
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DOI:
10.1155/2020/6075902
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发表时间:
2020
影响因子:
--
通讯作者:
Gao X
Gao X
中科院分区:
生物学3区
文献类型:
--
作者:
Hong W;Zhang Y;Ding J;Yang Q;Xie H;Gao X

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环状rna (circRNAs)在许多人类疾病,特别是癌症中起着至关重要的作用。circRNA HIPK3 (circHIPK3)是一种特殊的circRNA,可能参与非小细胞肺癌(non-small-cell lung cancer, NSCLC)的癌变,尽管其潜在的调控机制还不是很清楚。在这里,我们研究了circHIPK3在非小细胞肺癌中的作用。采用qRT-PCR法研究circHIPK3在NSCLC中的表达。通过沉默circHIPK3和miR-107模拟转染以及脑源性神经营养因子(BDNF)过表达来评估circHIPK3对NSCLC的影响,并通过双荧光素酶报告基因法评估circHIPK3、miR-107和BDNF之间的相关性。结果显示,circHIPK3在NSCLC细胞中表达上调。circHIPK3敲低通过促进miR-107的表达抑制NSCLC细胞的迁移和增殖。circHIPK3可作为miR-107海绵促进BDNF细胞增殖。双荧光素酶报告基因实验证明miR-107是circHIPK3的靶标,并且miR-107与BDNF的3 '非翻译区相互作用。miR-107过表达抑制bdnf介导的NSCLC细胞增殖。这些结果表明,circHIPK3通过新的circHIPK3/miR-107/BDNF轴促进肿瘤进展,这为非小细胞肺癌提供了潜在的标志物和药物治疗。
Circular RNAs (circRNAs) act as a crucial part in many human diseases, particularly in cancers. circRNA HIPK3 (circHIPK3) is a special circRNA that may participate in the oncogenesis of non-small-cell lung cancer (NSCLC), even though its latent regulatory mechanism is not very clear. Here, we studied the roles of circHIPK3 in NSCLC. qRT-PCR assay was applied to study the expression of circHIPK3 in NSCLC. The influence of circHIPK3 on NSCLC was estimated by silencing circHIPK3 and miR-107 mock transfection and brain-derived neurotrophic factor (BDNF) overexpression, and the correlation between circHIPK3, miR-107, and BDNF was evaluated by dual-luciferase reporter assay. The results showed that circHIPK3 expression was upregulated in NSCLC cells. circHIPK3 knockdown inhibited the migration and proliferation of NSCLC cells by promoting the expression of miR-107. circHIPK3 could be used as a miR-107 sponge to promote BDNF cell proliferation. The dual-luciferase reporter assay proved that miR-107 was the target of circHIPK3, and miR-107 had an interaction with the 3′untranslated region of BDNF. miR-107 overexpression inhibited BDNF-mediated NSCLC cell proliferation. These results indicate that circHIPK3 promotes tumor progression through a new circHIPK3/miR-107/BDNF axis, which offers potential markers and medical treatment for NSCLC.
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