China Oncology ›› 2020, Vol. 30 ›› Issue (1): 32-40.doi: 10.19401/j.cnki.1007-3639.2020.01.004

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Regulatory effect of miR-1290 targeting IRF2 on proliferation and invasion of non-small cell lung cancer cells and its related mechanism

DONG Lei 1 , ZHANG Zhongyan 2   

  1. 1. Department of Oncology, Wuhan Red Cross Hospital, Wuhan 430000, Hubei Province, China; 2. Department of Oncology and Traditional Chinese Medicine, Oncology Department, Chongqing University Affiliated Tumor Hospital, Chongqing 400030, China
  • Online:2020-01-30 Published:2020-01-17
  • Contact: ZHANG Zhongyan E-mail: kdfirei@sohu.com

Abstract:  Background and purpose: miR-1290 can regulate the expression of interferon regulatory factor-2 (IRF2) and the malignant biological behavior of non-small cell lung cancer (NSCLC), but the specific mechanism of its action is still unclear. Therefore, this study explored the regulatory effect of miR-1290 targeting IRF2 on the proliferation and invasion of NSCLC cells and its related mechanism. Methods: A549 cells cultured in vitro were divided into miR-1290 mimic group, miR-1290 inhibitor group and NC group. Real-time fluorescence quantitative polymerase chain reaction (RTFQ-PCR) and Western blot were performed to detect expression of miR-1290 and IRF2 in each group. Their targeted relationship was further verified by fluorescence assay. A549 cells cultured in vitro were divided into NC group (transfected with mimic), miR-1290 group (transfected with miR-1290), IRF2 group (transfected with IRF2) and miR-1290+IRF2 group (transfected with miR-1290+IRF2). Cell counting kit-8 (CCK-8) was performed to detect cell proliferation activity in each group. Transwell assay was performed to detect cell invasion in each group. The cell migration was detected by scratch test. The levels of vascular endothelial growth factor (VEGF), E-cadherin, matrix metalloproteinase (MMP)-2 and Ki-67 in each group were detected by Western blot. Results: IRF2 expression could be negatively regulated by miR-1290. Compared with NC group, miR-1290 expression was significantly up-regulated in miR-1290 group (P<0.05), while IRF2 expression was significantly down-regulated (P<0.05). Moreover, cell proliferation activity, invasion ability and migration rate were significantly increased (P<0.05), levels of VEGF, MMP-2 and Ki-67 were significantly up-regulated (P<0.05), and expression of E-cadherin was significantly down-regulated (P<0.05) in miR-1290 group. IRF2 expression was significantly up-regulated in IRF2 group (P<0.05), cell proliferation activity, invasion ability and migration rate were significantly decreased (P<0.05), levels of VEGF, MMP-2 and Ki-67 were significantly down-regulated (P<0.05), and protein level of E-cadherin was significantly up-regulated (P<0.05). Compared with IRF2 group, miR-1290 expression was significantly up-regulated in miR-1290+IRF2 group, while expression of IRF2 was significantly down-regulated (P<0.05). In addition, cell proliferation activity, invasion ability and migration rate were significantly increased (P<0.05), levels of VEGF, MMP-2 and Ki-67 were significantly up-regulated (P<0.05), and protein level of E-cadherin was significantly down-regulated (P<0.05). Conclusion: MiR-1290 may promote proliferation and invasion of NSCLC cells by negatively regulating IRF2 expression.

Key words: MiR-1290, Interferon regulatory factor-2, Non-small cell lung cancer