These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.
Pubmed for Handhelds
PUBMED FOR HANDHELDS
Search MEDLINE/PubMed
Title: LncRNA PCAT-1 promotes the progression of osteosarcoma via miR-508-3p/ZEB1 axis. Author: Chang L, Jia DL, Cao CS, Wei H, Li ZQ. Journal: Eur Rev Med Pharmacol Sci; 2021 Mar; 25(6):2517-2527. PubMed ID: 33829438. Abstract: OBJECTIVE: Osteosarcoma (OS) is an adolescent idiopathic malignancy with a poor prognosis. Accumulating evidence has verified that long non-coding RNAs (lncRNAs) were implicated in the initiation and development of various tumors. We aimed to clarify the functions and underlying mechanism of lncRNA PCAT-1 in OS progression. PATIENTS AND METHODS: RT-qPCR was performed to examine the relative expressions of PCAT-1, miR-508-3p and ZEB1 in OS tissues or cells. The proliferation capacities of OS cells with different transfection were detected by CCK-8 assays. Transwell assays were carried out to determine the functions of PCAT-1 and miR-508-3p in OS cell migration and invasion. Moreover, bioinformatical analysis and Luciferase reporter assay were applied to verify the association between PCAT-1 and miR-508-3p, miR-508-3p and ZEB1. RESULTS: Data of current study revealed that PCAT-1 was markedly upregulated in OS, which indicated poor prognosis of OS patients. CCK-8 and transwell assays indicated that PCAT-1 upregulation could promote OS cell proliferation, invasion and migration. Additionally, we found that miR-508-3p was a direct target of PCAT-1, and PCAT-1 regulated the development of OS via decreasing miR-508-3p and activating its target gene ZEB1. CONCLUSIONS: All data demonstrated that PCAT-1 promoted OS progression, and miR-508-3p/ZEB1 axis was implicated in the functional roles of PCAT-1 in OS, suggesting that PCAT-1/miR-508-3p/ZEB1 might serve as candidate therapeutic targets for OS patients.[Abstract] [Full Text] [Related] [New Search]