Downregulation of miR-588 is associated with tumor progression and unfavorable prognosis in patients with osteosarcoma

xlomafota13 shared this article with you from Inoreader Downregulation of miR-588 is associated with tumor progression and unfavorable prognosis in patients with osteosarcoma Via Experimental and therapeutic medicine Exp Ther Med. 2021 Jun;21(6):592. doi: 10.3892/etm.2021.10024. Epub 2021 Apr 8. ABSTRACT Osteosarcoma (OS) is a primary malignant tumor characterized by a high metastatic potential and poor prognosis. The dysregulation of miR-588 has been demonstrated to serve crucial roles in the progression of numerous types of cancer. The present study aimed to investigate the expression and function of miR-588 in the development of OS. To do so, clinical samples were collected and analyzed, and in vitro experiments were conducted. A total of 104 patients with OS were recruited between 2012 and 2014. The expression of miR-588 was analyzed by reverse transcription quantitative PCR. The association between miR-588 expression and the clinicopathological characteristics and survival rate of patients with OS was evaluated. Furthermore, Cell Counting Kit-8 and Transwell assays were used to evaluate the effect of miR-588 on the proliferation and the migrat ory and invasive abilities of various OS cell lines. The results demonstrated that miR-588 expression in OS tissues and cells was significantly lower compared with normal tissues and cells. In addition, miR-588 expression was closely associated with the Musculoskeletal Tumor Society (MSTS) staging of patients with OS. miR-588 expression and MSTS staging were therefore considered as independent indicators for the prognosis of patients with OS. In addition, miR-588 downregulation significantly stimulated the proliferation and migratory and invasive abilities of OS cells. Taken together, these findings indicated that miR-588 may serve as an independent prognostic factor and tumor suppressor in OS. PMID:33884030 | P MC:PMC8056108 | DOI:10.3892/etm.2021.10024 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.