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hsa_circ_0062389 promotes the progression of non-small cell lung cancer by sponging miR-103a-3p to mediate CCNE1 expression.
Cancer Genetics ( IF 1.9 ) Pub Date : 2019-12-18 , DOI: 10.1016/j.cancergen.2019.12.004
Yahui She 1 , Yuanyuan Han 1 , Guangting Zhou 1 , Fangyan Jia 1 , Tan Yang 1 , Zuojun Shen 2
Affiliation  

Recently, increasing evidence showed that circular RNAs (circRNAs) play critical roles in tumor progression. However, the roles of hsa_circ_0062389 in non-small cell lung cancer (NSCLC) development remain unclear. In the present study, hsa_circ_0062389 expression was significantly increased in NSCLC tissues and cell lines. High hsa_circ_0062389 expression was associated with advanced TNM stage and lymph-node metastasis. Function assays showed that hsa_circ_0062389 suppression reduced NSCLC cells proliferation and arrested cell cycle in G0/G1 phase. In mechanism, hsa_circ_0062389 directly interacted with miR-103a-3p in NSCLC, and CCNE1 acted as a target of miR-103a-3p. Furthermore, rescue assays showed that miR-103a-3p suppression or CCNE1 overexpression abolished the effects of hsa_circ_0062389 suppression on lung cancer cells progression. Therefore, our results showed that the hsa_circ_0062389/miR-103a-3p/CCNE1 axis might contribute to the tumorigenesis of NSCLC, which provided a new strategy for cancer treatment.



中文翻译:

hsa_circ_0062389通过掺入miR-103a-3p介导CCNE1表达来促进非小细胞肺癌的发展。

最近,越来越多的证据表明,环状RNA(circRNA)在肿瘤进展中起关键作用。但是,hsa_circ_0062389在非小细胞肺癌(NSCLC)发育中的作用仍不清楚。在本研究中,hsa_circ_0062389表达在NSCLC组织和细胞系中显着增加。hsa_circ_0062389高表达与晚期TNM分期和淋巴结转移有关。功能测定表明,hsa_circ_0062389抑制作用抑制了NSCLC细胞的增殖,并使细胞周期停滞在G0 / G1期。在机制上,hsa_circ_0062389与NSCLC中的miR-103a-3p直接相互作用,而CCNE1充当miR-103a-3p的靶标。此外,救援试验表明,miR-103a-3p抑制或CCNE1过表达消除了hsa_circ_0062389抑制对肺癌细胞进展的影响。

更新日期:2019-12-18
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