LncRNA FTX inhibition restrains osteosarcoma proliferation and migration via modulating miR-320a/TXNRD1.

It was well established that long non-coding RNAs (LncRNAs) could serve as oncogene or tumor suppressor in terms of the tumor type. FTX, as a member of lncRNA family, has been reported to be associated with several tumor progressions, such as hepatocellular carcinoma (HCC), renal cell carcinoma (RCC) and colorectal cancer. However, the regulatory role of FTX in osteosarcoma (OS) still lacks research analysis. This paper aims to explore how FTX exerts its regulatory role on OS by modulating TXNRD1/miR-320a, so as to provide a novel lncRNA theoretical framework for the diagnosis and treatment of OS. QRT-PCR revealed that FTX and TXNRD1 were abnormally upregulated in OS, whereas miR-320a expression was significantly decreased. Luciferase reporter analysis showed that both FTX and TXNRD1 could combine with miR-320a. A series of functional experiments indicated that knockdown of FTX could suppress OS cell proliferation and migration, while facilitating apoptosis ability simultaneously. However, TXNRD1 overexpression or miR-320a inhibition could rescue the oncogenic function of FTX. Taken all the experiment results together, this paper indicated that FTX impacted osteosarcoma cell proliferation and migration by modulating TXNRD1/miR-320a.