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Research Paper|Volume 12, Issue 24|pp 24957—24966

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

Quanxiao Xu1, Limin He1, Lei Ma1, Lin Fan2, Lihua Yan2, Xulin Zhao1, Yuanyuan Li1
  • 1Henan Medical Key Laboratory of Tumor Molecular Biology, Nanyang First People’s Hospital, Nanyang 473012, Henan Province, China
  • 2Department of Medical Oncology, Nanyang Second People's Hospital, Nanyang 473000, Henan, China
Received: February 21, 2020Accepted: May 27, 2020Published: December 19, 2020
https://doi.org/10.18632/aging.103464

Copyright: © 2020 Xu et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

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.