Long non‑coding RNA LINC00152 promotes tumorigenesis via sponging miR‑193b‑3p in osteosarcoma
- Pinduan Liu
- Wubin He
- Yanyan Lu
- Yue Wang
Affiliations: Department of Orthopedics, The First Affiliated Hospital of Jinzhou Medical University, Jinzhou, Liaoning 121001, P.R. China, Bio‑Therapeutics Laboratory, The First Affiliated Hospital of Jinzhou Medical University, Jinzhou, Liaoning 121001, P.R. China, Department of Oncology, The First Affiliated Hospital of Jinzhou Medical University, Jinzhou, Liaoning 121001, P.R. China
- Published online on: August 1, 2019 https://doi.org/10.3892/ol.2019.10700
Copyright: © Liu
et al. This is an open access article distributed under the
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The majority of the human genome has been revealed to be non‑protein‑coding, which are transcribed into noncoding RNAs (ncRNA), RNAs which are not translated into protein. Long non‑coding RNAs (lncRNAs), including LINC00152, may be associated with the pathogenesis of different types of cancer. LINC00152 serves as an endogenous sponge by binding to micro‑RNAs (miRNAs) and inhibiting their activity. The current study revealed that LINC00152 is overexpressed in osteosarcoma cells, leading to increased cell proliferation, and decreased G0/G1 cell cycle arrest and apoptosis. The binding of miR‑193b‑3p to LINC00152 was demonstrated by dual‑luciferase assay, and led to miR‑193b‑3p downregulation in osteosarcoma cells. Knockdown of LINC00152 revealed an antitumorigenic effect by reducing cell proliferation and increasing G0/G1 arrest and apoptosis. Inhibiting miR‑193b‑3p reversed the effects of LINC00152 knockdown. These results suggested that LINC00152 binds to miR‑193b‑3p and reduces its expression level, leading to increased cell proliferation and decreased G0/G1 cell cycle arrest and apoptosis in osteosarcoma cells.