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.

中文翻译：

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LncRNA FTX 抑制通过调节 miR-320a/TXNRD1 抑制骨肉瘤增殖和迁移。

众所周知，就肿瘤类型而言，长链非编码 RNA (LncRNA) 可以作为癌基因或肿瘤抑制基因。FTX 作为 lncRNA 家族的一员，据报道与多种肿瘤进展有关，如肝细胞癌 (HCC)、肾细胞癌 (RCC) 和结直肠癌。然而，FTX在骨肉瘤（OS）中的调节作用仍缺乏研究分析。本文旨在探讨FTX如何通过调节TXNRD1/miR-320a对OS发挥调控作用，为OS的诊治提供新的lncRNA理论框架。QRT-PCR 显示 FTX 和 TXNRD1 在 OS 中异常上调，而 miR-320a 表达显着降低。荧光素酶报告基因分析表明 FTX 和 TXNRD1 均可与 miR-320a 结合。一系列功能实验表明，敲低 FTX 可以抑制 OS 细胞增殖和迁移，同时促进细胞凋亡能力。然而，TXNRD1 过表达或 miR-320a 抑制可以挽救 FTX 的致癌功能。综合所有实验结果，本文表明 FTX 通过调节 TXNRD1/miR-320a 影响骨肉瘤细胞增殖和迁移。