Abstract
The aberrant expression of microRNAs (miRNAs/miRs) in osteosarcoma (OS) has been demonstrated in previous studies, and deregulation of miRNA expression has been associated with several types of cancer, including OS development and progression. Therefore, identifying the functional role of miRNAs in OS onset and development may facilitate the identification of novel and effective therapeutic targets for the treatment of patients with OS. Previous studies have demonstrated that miR-432 is involved in tumor formation and progression in several types of cancer. However, the expression pattern, functional role and underlying mechanism of miR-432 in OS remain unknown. In the current study, reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was used to measure miR-432 expression levels in OS tissue samples and cell lines. The effect of miR-432 overexpression on OS cell proliferation and invasion was detected using Cell Counting Kit-8 and Transwell invasion assays, respectively. Bioinformatics analysis was used to predict metastasis-associated in colon cancer 1 (MACC1) as a putative target of miR-432 and this was confirmed using a dual-luciferase reporter assay, RT-qPCR and western blot analysis. The current study demonstrated that miR-432 expression levels were significantly reduced in OS tissue samples and cell lines. In addition, functional assays revealed that overexpression of miR-432 significantly decreased OS cell proliferation and invasion. Furthermore, MACC1 was identified as a direct target gene of miR-432 in OS. MACC1 expression levels were significantly increased in OS tissue samples and an inverse correlation was observed between miR-432 and MACC1 expression in OS tissue samples. In addition, rescue experiments demonstrated that overexpression of MACC1 partially reversed the anti-proliferative and anti-invasive effects of miR-432 in OS cells. In conclusion, the present study demonstrated that miR-432 inhibited OS cell proliferation and invasion in vitro through direct targeting of MACC1, and miR-432 may be a potential therapeutic target for the treatment of OS.