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

circHIPK3 作为竞争性内源 RNA,通过 miR-107/BDNF 信号通路促进非小细胞肺癌的进展

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Abstract

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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