长链非编码RNA LEF1-AS1通过调节Wnt/β-catenin通路参与视网膜母细胞瘤的进展。

IF 2.5 4区 医学 Q3 PHARMACOLOGY & PHARMACY
Hua He, Mu Qin
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引用次数: 14

摘要

淋巴细胞增强子结合因子1反义RNA 1 (LEF1-AS1)已被认为在几种类型的人类癌症中作为肿瘤相关的lncRNA发挥作用,但迄今为止还没有关于LEF1-AS1在视网膜母细胞瘤中的作用的研究。在我们的研究中,LEF1-AS1在视网膜母细胞瘤组织和细胞系中的表达分别高于配对相邻的正常组织和视网膜色素上皮细胞系。同时,我们发现IIRC D-E型或未分化型视网膜母细胞瘤患者的LEF1-AS1表达水平明显高于IIRC A-C型或分化型。高表达的LEF1-AS1预示着视网膜母细胞瘤患者较差的无病生存期。体外实验表明,沉默LEF1-AS1可通过调节Wnt/β-catenin通路抑制视网膜母细胞瘤细胞的增殖、迁移和侵袭。综上所述,LEF1-AS1在视网膜母细胞瘤中发挥着致癌lncRNA的作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Long non-coding RNA LEF1-AS1 is involved in the progression of retinoblastoma through regulating the Wnt/β-catenin pathway.

The lymphoid enhancer binding factor 1 antisense RNA 1 (LEF1-AS1) has been suggested to function as a tumour-associated lncRNA in several types of human cancers, but there is no study to date about the role of LEF1-AS1 in retinoblastoma. In our study, LEF1-AS1 expression was increased in retinoblastoma tissues and cell lines compared with paired adjacent normal tissues and the retinal pigment epithelial cell line, respectively. Meanwhile, we found that patients with retinoblastoma with IIRC D-E or undifferentiated type had notably higher levels of LEF1-AS1 expression than those with IIRC A-C or differentiated type. High LEF1-AS1 expression predicted poor disease-free survival in patients with retinoblastoma. The in vitro assays suggested that silencing of LEF1-AS1 suppressed retinoblastoma cell proliferation, migration, and invasion through regulating the Wnt/β-catenin pathway. In conclusion, LEF1-AS1 functions as an oncogenic lncRNA in retinoblastoma.

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来源期刊
Clinical and Experimental Pharmacology and Physiology
Clinical and Experimental Pharmacology and Physiology PHARMACOLOGY & PHARMACY-PHYSIOLOGY
自引率
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128
期刊介绍: Clinical and Experimental Pharmacology and Physiology is an international journal founded in 1974 by Mike Rand, Austin Doyle, John Coghlan and Paul Korner. Our focus is new frontiers in physiology and pharmacology, emphasizing the translation of basic research to clinical practice. We publish original articles, invited reviews and our exciting, cutting-edge Frontiers-in-Research series’.
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