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

Xiaodong Huo,Lili Wang,Huixing Wang,Haitao Wang,Kuo Yang,Bin Huo,Jinhuan Wang,Lei Wang

doi:10.1186/s12935-020-1130-5

Xiaodong Huo, Lili Wang + Show 6 more

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https://doi.org/10.1186/s12935-020-1130-5

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Abstract

BackgroundExtensive 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.MethodsRT-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.ResultsRT-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.ConclusionFTX played an oncogenic role in LUAD and contributed to cancer development via targeting miR-335-5p/NUCB2 axis.

Highlights

Extensive studies revealed that long non-coding RNAs could act as a regulator in tumors, including lung adenocarcinoma (LUAD)
(EMT) process is closely correlated with cell migration and invasion [16, 17], we evaluated whether FTX transcript (FTX) could induce Epithelial–mesenchymal transition (EMT) in LUAD cells
It was well known that cell proliferation and apoptosis are the important processes involved in cancer progression

Summary

Introduction

Extensive studies revealed that long non-coding RNAs (lncRNAs) could act as a regulator in tumors, including lung adenocarcinoma (LUAD). Lung cancer is one of the most aggressive tumors and its incidence and mortality demonstrated a swift growth in recent decades [1]. It can be histologically divided into small cell lung carcinoma (SCLC) and non-small cell lung carcinoma (NSCLC). Previous studies showed that lncRNA could function as a competing endogenous RNA (ceRNA) and affect cancer progression by sponging microRNAs (miRNAs) to release messenger RNAs (mRNAs) at post-transcriptional level [9, 10]. LncRNA CDKN2BAS serves as a ceRNA in hepatocellular carcinoma and predicts poor prognosis via regulating miR-153-5p/ARHGAP18 axis [12]

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