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LINC01410 accelerated the invasion and proliferation of osteosarcoma by sponging miR-3128

Increasing evidence has shown that lncRNAs are closely correlated with cell apoptosis, autophagy and progression. However, the role of LINC01410 in osteosarcoma has not been verified. We determined that LINC01410 was overexpressed in osteosarcoma specimens and cell lines. The expression of LINC01410...

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Detalles Bibliográficos
Autores principales: Xu, Quanxiao, He, Limin, Ma, Lei, Fan, Lin, Yan, Lihua, Zhao, Xulin, Li, Yuanyuan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Impact Journals 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7803582/
https://www.ncbi.nlm.nih.gov/pubmed/33401246
http://dx.doi.org/10.18632/aging.103464
Descripción
Sumario:Increasing evidence has shown that lncRNAs are closely correlated with cell apoptosis, autophagy and progression. However, the role of LINC01410 in osteosarcoma has not been verified. We determined that LINC01410 was overexpressed in osteosarcoma specimens and cell lines. The expression of LINC01410 was upregulated in 22 osteosarcoma patients (22/30, 73%) compared to control normal samples. Ectopic expression of LINC01410 promoted the osteosarcoma cell cycle, proliferation and invasion. Overexpression of LINC01410 induced N-cadherin and Vimentin expression and inhibited E-cadherin expression in osteosarcoma cells. LINC01410 acted as a sponge for miR-3128. The results showed that miR-3128 overexpression decreased the luciferase activity of WT-LINC01410 but not mut-LINC01410 in MG-63 cells. Upregulation of LINC01410 expression suppressed miR-3128 expression in MG-63 cells. Moreover, LINC01410 overexpression increased osteosarcoma cell invasion and growth by modulating miR-3128. These data indicated that LINC01410 acted as an oncogene in osteosarcomagenesis and might be a potential new strategy for osteosarcoma treatment.