She Yahui, Han Yuanyuan, Zhou Guangting, Jia Fangyan, Yang Tan, Shen Zuojun
Clinical Laboratory, People's Hospital of Bozhou City, BoZhou, Anhui 236800, China.
Anhui Provincial Center for Clinical Laboratories, No. 17 Lujiang Road, Hefei, Anhui 230001, China.
Cancer Genet. 2020 Feb;241:12-19. doi: 10.1016/j.cancergen.2019.12.004. Epub 2019 Dec 18.
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.
最近，越来越多的证据表明，环状RNA（circRNAs）在肿瘤进展中起关键作用。然而，hsa_circ_0062389在非小细胞肺癌（NSCLC）发生发展中的作用仍不清楚。在本研究中，hsa_circ_0062389在NSCLC组织和细胞系中的表达显著增加。hsa_circ_0062389高表达与晚期TNM分期和淋巴结转移相关。功能分析表明，hsa_circ_0062389的抑制降低了NSCLC细胞的增殖，并使细胞周期停滞在G0/G1期。机制上，hsa_circ_0062389在NSCLC中直接与miR-103a-3p相互作用，而CCNE1是miR-103a-3p的靶标。此外，挽救实验表明，miR-103a-3p的抑制或CCNE1的过表达消除了hsa_circ_0062389抑制对肺癌细胞进展的影响。因此，我们的结果表明，hsa_circ_0062389/miR-103a-3p/CCNE1轴可能促进NSCLC的肿瘤发生，这为癌症治疗提供了一种新策略。
