ArticleExperimental and therapeutic medicine2018
MicroRNA-466 inhibits osteosarcoma cell proliferation and induces apoptosis by targeting CCND1.
Article in Experimental and therapeutic medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- The Clinical Significance and Functional Role of miR-466 in Gastric Cancer Peritoneal Metastasis.Molecular biotechnology · 2022Article
- SLC25A10 performs an oncogenic role in human osteosarcoma.Oncology letters · 2020Article
- MicroRNAs signatures, bioinformatics analysis of miRNAs, miRNA mimics and antagonists, and miRNA therapeutics in osteosarcoma.Cancer cell international · 2020Review
- Knockdown of CYP19A1 in Buffalo Follicular Granulosa Cells Results in Increased Progesterone Secretion and Promotes Cell Proliferation.Frontiers in veterinary science · 2020Article
- LINC00355 promoted the progression of lung squamous cell carcinoma through regulating the miR-466/LYAR axis.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2020Article
- miR-466 and NUS1 Regulate the AKT/Nuclear Factor kappa B (NFκB) Signaling Pathway in Intrauterine Adhesions in a Rat Model.Medical science monitor : international medical journal of experimental and clinical research · 2019Article
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Authors and funding
5 authors.
Funding
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Abstract
Emerging pieces of evidence indicate that microRNA-466 (miR-466) serves as a tumor suppressor in several human tumors, including colorectal cancer and prostate cancer. However, whether miR-466 is involved in osteosarcoma (OS) progression remains largely unknown. The present study demonstrated that miR-466 was significantly downregulated in OS tissues and cell lines. Furthermore, it was revealed that the expression of miR-466 was negatively correlated with OS severity. Moreover, low miR-466 expression in patients with OS predicted poor prognosis. Through functional experiments, miR-466 overexpression significantly inhibited the proliferation and cell cycle of OS cells while inducing cellular apoptosis. In terms of mechanism, it was revealed that CCND1 was a target of miR-466 in OS cells. miR-466 overexpression suppressed CCND1 expression in OS cells. A reverse association was observed between the expression levels of miR-466 and CCND1 in OS tissues. Furthermore, CCND1 restoration in OS cells significantly rescued the effects of miR-466 on cellular proliferation and apoptosis. Overall, the results of the present study demonstrated that miR-466 suppressed OS progression by targeting CCND1, suggesting that miR-466 may be a promising biomarker and therapeutic target for OS prognosis and treatment.
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Registered trials
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