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Abstract
Osteosarcoma (OS) is a common kind of aggressive tumor in bone which was mostly identified
in children and adolescents with extremely high risk of death. Accumulating research
works have displayed that long noncoding RNAs (lncRNAs) exert an essential role in
the development of multiple cancers. It has been reported that TMPO-AS1 is an oncogene
in cancers; nonetheless, its molecular mechanism in OS is totally unclear. Our present
study elucidated that a remarkable overexpression of TMPO-AS1 was found in OS tissues
and cells. Moreover, TMPO-AS1 depletion restrained Wnt/β-catenin pathway and cell
proliferation as well as facilitated cell apoptosis. Further molecular mechanism investigations
showed that TMPO-AS1 can sponge to miR-199a-5p. Moreover, miR-199a-5p was at a low
level at OS cells. Importantly, miR-199a-5p's overexpression was associated with the
OS cells' decreased proliferation and increased apoptosis. In addition, WNT7B was
confirmed as a downstream gene of miR-199a-5p. Also the WNT7B expression was reversely
modulated by miR-199a-5p and positively modulated by TMPO-AS1. Rescue experiments
suggested that downregulated WNT7B rescued miR-199a-5p inhibitor-mediated repression
on OS progression, but the treatment of LiCl counteracted the effect of WNT7B downregulation.
In a word, TMPO-AS1 serves as a competing endogenous RNA to boost osteosarcoma tumorigenesis
by regulating miR-199a-5p/WNT7B axis, which provided an underlying therapeutic target
for patients with OS.