4.6 Article

MicroRNA-32-5p inhibits epithelial-mesenchymal transition and metastasis in lung adenocarcinoma by targeting SMAD family 3

期刊

JOURNAL OF CANCER
卷 12, 期 8, 页码 2258-2267

出版社

IVYSPRING INT PUBL
DOI: 10.7150/jca.48387

关键词

non-small cell lung cancer; microRNA-32-5p; SMAD3; migration; invasion

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资金

  1. National Natural Science Foundation of China [81701802]

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The study found that miR-32-5p is downregulated in NSCLC tissues and inhibits the migration and invasion abilities of tumors by targeting SMAD3. miR-32-5p may be a potential therapeutic target for the treatment of lung adenocarcinoma.
Non-small cell lung cancer (NSCLC) is the leading cause of cancer-associated death worldwide. MicroRNA (miRNA)-32-5p is as an important cancer-associated miRNA in different types cancer. To date, the role of miR-32-5p in the migration and invasion of NSCLC remains unknown. In the present study, a Transwell assay was performed to investigate the role of miR-32-5p in lung adenocarcinoma. miR-32-5p expression level was determined via reverse transcription-quantitative PCR in 24 pairs of NSCLC and adjacent normal tissues. SMAD family member 3 (SMAD3) was considered as a novel target gene by luciferase reporter assay and western blot in NSCLC. The present study demonstrated that miR-32-5p is frequently downregulated in NSCLC tissues. The overexpression of miR-32-5p resulted in the inhibition of migratory and invasive abilities in NSCLC cells. Thus, SMAD3 was identified as a target of miR-32-5p, and its expression was negatively correlated with miR-32-5p expression in clinical NSCLC tissues. Overall, these findings indicate that miR-32-5p serves as a tumor suppressor by targeting SMAD3. Thus, miR-32-5p may be a potential therapeutic target for the treatment of lung adenocarcinoma.

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