Long noncoding RNA FEZF1-AS1 promotes the motility of esophageal squamous cell carcinoma through Wnt/β-catenin pathway

Long noncoding RNA FEZF1-AS1 promotes the motility of esophageal squamous cell carcinoma through Wnt/β-catenin pathway
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长链非编码RNA FEZF1-AS1通过Wnt/β-catenin通路促进食管鳞癌的运动

DOI:
10.2147/cmar.s196004
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发表时间:
2019-01-01
影响因子:
3.3
通讯作者:
He, Fucheng
He, Fucheng
中科院分区:
医学4区
文献类型:
--
作者:
Yang, Lijun;Ye, Yafei;He, Fucheng

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背景:长非编码RNA(Long Non Coding RNAs,LncRNAs)是一类非编码的RNA核苷酸,在肿瘤的发生发展中起重要作用。FEZ家族锌指1反义RNA1(FEZF1-AS1)是一种在某些肿瘤中具有促癌作用的lncRNA。然而,其在食管鳞癌中的作用及其可能的调控机制目前尚不清楚。方法:采用定量逆转录聚合酶链式反应检测FEZF1-AS1和CTNNB1(β-catenin)在食管鳞癌组织和细胞中的表达水平。细胞转染实验下调或过表达FEZF1-AS1在EC1和EC9706细胞中的表达。采用WST-1实验、细胞周期实验、划痕实验、迁移和侵袭实验评价FEZF1-AS1在食管癌发生发展过程中的作用。沉默FEZF1-AS1显著抑制ESCC细胞的迁移和侵袭,而过表达FEZF1-AS1显著促进ESCC的迁移和侵袭。同时,FEZF1-AS1的表达水平对ESCC细胞的增殖和细胞周期无影响。我们还发现,β-连环蛋白在食管鳞癌组织中表达上调,其水平与FEZF1-AS1的表达呈正相关。沉默FEZF1-AS1可以降低β-连环素的mRNA和蛋白水平,而过表达FEZF1-AS1可以导致相反的结果。结论:lncRNA FEZF1-AS1的表达在ESCC的发展过程中起着重要作用,尤其是在肿瘤的运动中。FEZF1-AS1可能为ESCC的治疗提供了新的视角。
Background: Long noncoding RNAs (lncRNAs), a class of noncoding RNA nucleotides >200 bp, has been demonstrated to play vital role in the development of cancer. FEZ family zinc finger 1 antisense RNA 1 (FEZF1-AS1) has been reported as an lncRNA which acts as a tumor-promoting effect in some cancers. However, the role of it in esophageal squamous cell carcinoma (ESCC) and its potential regulatory mechanism was unclear now.Methods: qRT-PCR was used to detect the levels of FEZF1-AS1 and mRNA CTNNB1 (beta-catenin) in ESCC tissues and cells. Cell transfection experiments were used to knock down or overexpress the level of FEZF1 -AS1 in EC1 and EC9706 cell lines. WST-1 assays, cell cycle assays, scratch wound assays, migration, and invasion assays were used to evaluate the function of FEZF1-AS1 in ESCC progression.Results: FEZF1-AS1 was remarkably upregulated in ESCC tissues and cell lines. Silencing of FEZF1-AS1 significantly inhibited the migration and invasion of ESCC cells, while overexpression of FEZF1-AS1 notably accelerated ESCC migration and invasion. Meanwhile, the levels of FEZF1-AS1 had no effect on ESCC cell proliferation and cell cycle. We also found that beta-catenin was upregulated in ESCC tissues, and the level of it was positively correlated with the expression of FEZF1 -AS1. Silencing of FEZF1-AS1 could decrease the mRNA and protein level of beta-catenin, while overexpression FEZF1-AS1 could lead to the contrary.Conclusion: Our results suggested that the expression of lncRNA FEZF1-AS1 played an important role in ESCC progression, especially the motility of the tumor. FEZF1-AS1 may provide us with a new sight for ESCC treatment.