J Cancer 2021; 12(8):2258-2267. doi:10.7150/jca.48387
MicroRNA-32-5p inhibits epithelial-mesenchymal transition and metastasis in lung adenocarcinoma by targeting SMAD family 3
Department of Interventional Radiology, The First Affiliated Hospital of Nanjing Medical University; Gulou, Nanjing 210029, P.R. China.
*These authors contributed equally to this work.
Zhang JX, Yang W, Wu JZ, Zhou C, Liu S, Shi HB, Zhou WZ. MicroRNA-32-5p inhibits epithelial-mesenchymal transition and metastasis in lung adenocarcinoma by targeting SMAD family 3. J Cancer 2021; 12(8):2258-2267. doi:10.7150/jca.48387. Available from https://www.jcancer.org/v12p2258.htm
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.
Keywords: non-small cell lung cancer, microRNA-32-5p, SMAD3, migration, invasion