Abstract. MicroRNAs (miRNA/miRs) have been associated with the initiation and progression of non-small-cell lung cancer (NSCLC). Hence, a comprehensive understanding of the association between dysregulated miRNAs and NSCLC may contribute to the identification of novel therapeutic methods for patient

NIAN LIU,ZHIGUANG LIU,WEIDONG ZHANG,LI YANG, JUN CAO, HUAN YANG, LI XIUYING

semanticscholar(2018)

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摘要
MicroRNAs (miRNA/miRs) have been associated with the initiation and progression of non-small-cell lung cancer (NSCLC). Hence, a comprehensive understanding of the association between dysregulated miRNAs and NSCLC may contribute to the identification of novel therapeutic methods for patients with NSCLC. MiRNA-433 (miR-433) has been reported to be dysregulated in numerous types of human cancers; however, its expression pattern, biological roles and associated mechanisms in NSCLC require further investigation. The present study aimed to detect miR-433 expression and determine its roles and underlying molecular mechanisms in NSCLC. In the present study, reverse transcription-quantitative polymerase chain reaction revealed that miR-433 was significantly downregulated in NSCLC tissues and cell lines. This decreased miR-433 expression was strongly associated with the tumor node metastasis stage and lymph node metastasis of patients with NSCLC. Cell Counting kit-8 and cell invasion assays revealed that the resumption of miR-433 expression decreased the proliferation and invasion of NSCLC cells. Bioinformatics analysis predicted E2F transcription factor 3 (E2F3) as a potential target of miR-433. Luciferase reporter assay, RT-qPCR and western blot analysis further demonstrated that E2F3 was a direct target of miR-433 in NSCLC. E2F3 downregulation induced by small interfering RNA exhibited inhibitory effects similar to those of miR-433 overexpression in NSCLC cells, and the restored E2F3 expression counteracted the suppressive effects on NSCLC cells induced by miR-433 overexpression. Therefore, miR-433 may inhibit the progression of NSCLC, at least in part, by targeting E2F3. The present study indicated that miR-433 may be investigated as an innovative candidate target for the therapy of patients with this fatal disease.
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