Open AccessMicroRNA-454 inhibits non‑small cell lung cancer cells growth and metastasis via targeting signal transducer and activator of transcription-3
Author(s) -
Shuliang Liu,
Xingping Ge,
Lingfei Su,
Aifeng Zhang,
Xuri Mou
Publication year - 2017
Publication title -
molecular medicine reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.727
H-Index - 56
eISSN - 1791-3004
pISSN - 1791-2997
DOI - 10.3892/mmr.2017.8350
Subject(s) - microrna , cancer research , lung cancer , oncogene , biology , gene knockdown , cell cycle , metastasis , stat3 , cell growth , stat protein , downregulation and upregulation , molecular medicine , cancer , apoptosis , oncology , medicine , gene , genetics
Lung cancer is one of the most common type of cancers and the leading cause of cancer‑related mortality worldwide. Non-small cell lung cancer (NSCLC) accounts for >80% of lung cancer cases. Emerging studies have suggested that microRNAs are dysregulated in NSCLC and serve important roles in NSCLC initiation and development. However, to the best of our knowledge, the expression, roles and molecular mechanism of microRNA‑454 (miR‑454) have not been investigated in NSCLC. In the present study, miR‑454 was demonstrated to be significantly downregulated in NSCLC tissues and cell lines, as assessed by western blot analysis and reverse transcription‑quantitative polymerase chain reaction. Reduced miR‑454 expression was significantly correlated with aggressive clinicopathological features in NSCLC. In addition, upregulation of miR‑454 suppressed proliferation, migration and invasion NSCLC cells, as assessed by Cell Counting Kit‑8 and in vitro migration and invasion assays, respectively. Furthermore, bioinformatics analysis identified STAT3 as a direct target gene of miR‑454, and STAT3 knockdown was demonstrated to simulate the effects of miR‑454 overexpression in NSCLC. In conclusion, the present study provided convincing evidence that miR‑454 is downregulated in NSCLC, and regulates growth and metastasis by directly targeting STAT3, which suggests that miR‑454 may be an efficient therapeutic target for NSCLC.