Long non-coding RNA ATB promotes human non-small cell lung cancer proliferation and metastasis by suppressing miR-141-3p.

Guojie Lu,Yaosen Zhang,Klaus Roemer

doi:10.1371/journal.pone.0229118

Guojie Lu, Yaosen Zhang + Show 1 more

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https://doi.org/10.1371/journal.pone.0229118

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Journal: PloS one	Publication Date: Feb 24, 2020
Citations: 8	License type: CC BY 4.0

Affiliation: Panyu District Central Hospital

Abstract

Long noncoding RNA activated by transforming growth factor-β (lncRNA-ATB) plays a critical role in progression of several cancers. In this study, lncRNA-ATB was significantly up-regulated in NSCLC tissues and cell lines, and high lncRNA-ATB expression indicated poor prognosis. Knockdown of lncRNA-ATB suppressed NSCLC cell growth, colony formation, migration, invasion and reversed epithelial-mesenchymal transition. In vivo study showed that silencing lncRNA-ATB inhibited tumor growth. Further mechanism studies demonstrated that lncRNA-ATB was a target of miR-141-3p. MiR-141-3p expression was negatively related to lncRNA-ATB expression in NSCLC tissues. These results suggested that inhibiting lncRNA-ATB might be an approach for NSCLC treatment.

Highlights

Lung cancer is one of the most frequently diagnosed tumors, which ranks the third most common in the world
The Kaplan-Meier survival analysis showed that the high Long non-coding RNA (lncRNA)-ATB was associated with poor prognosis in patients with Non-small cell lung cancer (NSCLC) (P < 0.05, Fig 1C)
Xiong et al found that higher expression of lncRNA-ATB was observed in renal cell carcinoma tissues and renal cancer cell lines than that in adjacent normal kidney tissues and normal human proximal tubule epithelial cell line HK-2

Summary

Introduction

Lung cancer is one of the most frequently diagnosed tumors, which ranks the third most common in the world. Non-small cell lung cancer (NSCLC) is the most common type of lung cancer, accounting for about 80% of all cases [1]. The overall 5-year survival rate of NSCLC patients still remains poor, despite substantial advances achieved in the treatment [2,3,4]. Better understanding of the underlying pathological mechanisms will contribute to develop more effective therapeutic strategies, thereby improving the clinical outcome of NSCLC patients. The regulation of the non-protein-coding genome in normal physiology and the pathogenesis of diseases including NSCLC have attracting growing intention [8, 9]

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