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

Huang, Shuaihao; Zhu, Xiaowen; Yu-hong, KE; Xiao, Dan; Liang, Changxiang; Chen, Junfeng; Chang, Yunbing

doi:10.1080/15384047.2019.1702405

Cited by 39 publications

(27 citation statements)

References 24 publications

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“…Specifically, numerous miRNAs, participating in LUAD development, were reported to be regulated by lncRNAs [26][27][28]. FTX has been supported as a ceRNA in several tumors, such as hepatocellular carcinoma [29], osteosarcoma [30] and colorectal cancer [14]. Herein, our present study first showed that FTX was a cytoplasmic RNA and interacted with miR-335-5p in LUAD.…”

Section: Discussionmentioning

confidence: 49%

FTX contributes to cell proliferation and migration in lung adenocarcinoma via targeting miR-335-5p/NUCB2 axis

et al. 2020

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Background: Extensive studies revealed that long non-coding RNAs (lncRNAs) could act as a regulator in tumors, including lung adenocarcinoma (LUAD). LncRNA FTX transcript, XIST regulator (FTX) has been reported to regulate the biological behaviors of some cancers. Nevertheless, its functional role and molecular mechanism remain obscure in LUAD. Our current study concentrates on exploring the biological function of FTX in LUAD. Methods: RT-qPCR was used to test the expression of FTX, miR-335-5p or NUCB2 in LUAD cells. The effect of FTX on LUAD progression was investigated by colony formation, EdU, flow cytometry, TUNEL, transwell and western blot assays. The interaction between microRNA-335-5p (miR-335-5p) and FTX or nucleobindin 2 (NUCB2) was confirmed by luciferase reporter assay. Results: RT-qPCR showed that FTX expression was up-regulated in LUAD cell lines. Loss-of-function assay indicated that FTX accelerated cell proliferation, migration and invasion, while inhibited cell apoptosis in LUAD. Besides, miR-335-5p, lowly expressed in LUAD cells, was discovered to be sponged by FTX. Subsequently, NUCB2 was identified as a target gene of miR-335-5p. Additionally, it was confirmed that NUCB2 functioned as an oncogene in LUAD. Rescue assays indicated that LUAD progression inhibited by FTX knockdown could be restored by NUCB2 up-regulation. Conclusion: FTX played an oncogenic role in LUAD and contributed to cancer development via targeting miR-335-5p/NUCB2 axis.

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Section: Discussionmentioning

confidence: 49%

FTX contributes to cell proliferation and migration in lung adenocarcinoma via targeting miR-335-5p/NUCB2 axis

et al. 2020

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“…LncRNA FTX was firstly identified in XIST gene locus and was dysregulated in many human cancers [ 15 , 35 , 36 ]. FTX is located upstream of XIST , within the X-inactivation center, and produces a spliced lncRNA which positively regulate the expression of XIST , which is essential for initiation and spread of X-inactivation (provided by RefSeq, May 2015).…”

Section: Discussionmentioning

confidence: 99%

RMRP, RMST, FTX and IPW: novel potential long non-coding RNAs in medullary thyroid cancer

Lasa

Villalba‐Benito

Fernández

et al. 2021

Orphanet J Rare Dis

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The relevant role of long non-coding RNAs (lncRNAs) in cancer is currently a matter of increasing interest. Medullary thyroid cancer (MTC) is a rare neuroendocrine tumor (2–5% of all thyroid cancer) derived from the parafollicular C-cells which secrete calcitonin. About 75% of all medullary thyroid cancers are believed to be sporadic medullary thyroid cancer (sMTC), whereas the remaining 25% correspond to inherited cancer syndromes known as Multiple Endocrine Neoplasia type 2 (MEN2). MEN2 syndrome, with autosomal dominant inheritance is caused by germline gain of function mutations in RET proto-oncogene. To date no lncRNA has been associated to MEN2 syndrome and only two articles have been published relating long non-coding RNA (lncRNA) to MTC: the first one linked MALAT1 with sMTC and, in the other, our group determined some new lncRNAs in a small group of sMTC cases in fresh tissue (RMST, FTX, IPW, PRNCR1, ADAMTS9-AS2 and RMRP). The aim of the current study is to validate such novel lncRNAs previously described by our group by using a larger cohort of patients, in order to discern their potential role in the disease. Here we have tested three up-regulated (RMST, FTX, IPW) and one down-regulated (RMRP) lncRNAs in our samples (formalin fixed paraffin embedded tissues from twenty-one MEN2 and ten sMTC patients) by RT-qPCR analysis. The preliminary results reinforce the potential role of RMST, FTX, IPW and RMRP in the pathogenesis of MTC.

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“…The mechanisms of promoting cancer by FTX may be involved in the following aspects.FTX signi cantly promoted proliferation and invasion of glioma cells by negatively regulating miR-342-3p [24]; FTX exerted its oncogenic role in OSC via up-regulating the expression of TXNRD1 through sponging miR-320a [25];…”

Section: Discussionmentioning

confidence: 99%

Long non-coding RNA FTX predicts a poor prognosis of human cancers: a meta-analysis

Chen

Guo

et al. 2020

Preprint

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Background Several studies assessed the relationship between FTX expression level and clinicopathological features and survival outcomes in patients with cancer, but these results were conflicting. This meta-analysis aimed to synthesize existing data to clarify the association of FTX with prognosis of cancers. Methods Electronic databases of PubMed, Embase, Cochrane library, Web of Science, Chinese CNKI, and the Chinese WanFang databases were used to search for relevant studies. Role of FTX in cancers was evaluated by pooled odds ratios (ORs) and hazard ratios (HRs) with 95% confidence intervals (CIs). Results In total, 11 studies compromising 1210 participants including colorectal cancer (CRC), hepatocellular carcinoma (HCC), gastric cancer (GC), renal cell carcinoma (RCC), osteosarcoma (OSC), and glioma, were enrolled in this analysis. The meta-analysis showed that high FTX expression was associated with lymph node metastasis, distant metastasis, tumor size and TNM/clinical stage. More importantly, the pooled results from survival analysis revealed that there was a significant correlation between high FTX expression and a shorter OS in patients with HCC, CRC, GC, OSC, and glioma, and that FTX overexpression could be an independent predictive marker for shorter OS in patients with CRC, HCC, OSC, and glioma. Conclusions FTX may be a potential oncogene, and high FTX expression be associated with a poor prognosis in patients with CRC, HCC, OSC, and glioma.

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

Cited by 39 publications

References 24 publications

FTX contributes to cell proliferation and migration in lung adenocarcinoma via targeting miR-335-5p/NUCB2 axis

FTX contributes to cell proliferation and migration in lung adenocarcinoma via targeting miR-335-5p/NUCB2 axis

RMRP, RMST, FTX and IPW: novel potential long non-coding RNAs in medullary thyroid cancer

Long non-coding RNA FTX predicts a poor prognosis of human cancers: a meta-analysis

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