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miR-454-3p inhibits non-small cell lung cancer cell proliferation and metastasis by targeting TGFB2

Accumulating studies have suggested that microRNAs (miRs) play a significant role in lung cancer development and progression, especially in non-small cell lung cancer (NSCLC). The present study aimed to investigate the associations between miR-454-3p and NSCLC progression. qPCR assay was applied to...

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Detalles Bibliográficos
Autores principales: Liao, Hongliang, Liang, Yaqin, Kang, Lin, Xiao, Yun, Yu, Tao, Wan, Renping
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8020204/
https://www.ncbi.nlm.nih.gov/pubmed/33760169
http://dx.doi.org/10.3892/or.2021.8018
Descripción
Sumario:Accumulating studies have suggested that microRNAs (miRs) play a significant role in lung cancer development and progression, especially in non-small cell lung cancer (NSCLC). The present study aimed to investigate the associations between miR-454-3p and NSCLC progression. qPCR assay was applied to examine the expression of miR-454-3p and transforming growth factor-β2 (TGFB2) in tissues and cell lines. CCK-8 and EdU assays were used to detect cell proliferation. Wound-healing and Transwell assays were conducted to assess cell migration and invasion. Western blotting assay was performed to explore the protein levels of epithelial-mesenchymal transition (EMT) markers. The interaction between miR-454-3p and TGFB2 was investigated with a luciferase reporter assay. miR-454-3p was downregulated in NSCLC tissues and NSCLC cell lines. miR-454-3p overexpression led to the suppression of proliferation, migration, and invasion in A549 and NCI-H1650 cells. In addition, the overexpression of miR-454-3p in A549 and NCI-H1650 cells significantly inhibited EMT. TGFB2 was revealed to be a direct target of miR-454-3p by using TargetScan database and luciferase reporter assay. TGFB2 was observed to be upregulated in NSCLC tissues and cell lines. Further mechanistic studies revealed that the inhibitory effects of miR-454-3p on NSCLC were reversed upon overexpression of TGFB2. These findings provided strong evidence that miR-454-3p suppressed NSCLC cell proliferation and metastasis by targeting TGFB2. The study suggests that targeting miR-454-3p could be a promising strategy for treating NSCLC.