Retraction: Overexpression of long non-coding RNA SBF2-AS1 promotes cell progression in esophageal squamous cell carcinoma (ESCC) by repressing miR-494 to up-regulate PFN2 expression.

IF 1.8 4区 生物学 Q3 BIOLOGY Biology Open Pub Date : 2025-01-15 Epub Date: 2025-01-24 DOI:10.1242/bio.048793
Qiu Zhang, Xixiang Pan, Dongyang You
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长非编码 RNA SBF2-AS1 的过表达会抑制 miR-494 上调 PFN2 的表达,从而促进食管鳞状细胞癌(ESCC)的细胞进展。
食管鳞状细胞癌(ESCC)是一种因吸烟、饮酒和营养不良而导致的难治性食管癌。最近,长非编码 RNA SET 结合因子 2 反义 RNA 1(SBF2-AS1)被证实是多种癌症的致癌基因。然而,SBF2-AS1在ESCC进展中的作用机制尚不清楚。本研究采用实时聚合酶链式反应(qRT-PCR)方法发现,在 ESCC 肿瘤和细胞中,SBF2-AS1 和 PFN2 的表达上调,而 miR-494 的表达下调。3-(4,5-二甲基-2-噻唑基)-2,5-二苯基-2-H-溴化四氮唑(MTT)试验和透孔试验表明,沉默SBF2-AS1可抑制增殖、迁移和侵袭。此外,Western 印迹显示,通过检测 MMP9、Vimentin 和 E-cadherin 蛋白表达,SBF2-AS1 基因缺失还抑制了上皮细胞向间充质转化(EMT)。我们通过荧光素酶报告系统、RIP和RNA牵引实验证实了miR-494是SBF2-AS1的靶标。此外,miR-494抑制剂逆转了SBF2-AS1沉默对ESCC细胞增殖、迁移、侵袭和EMT的抑制作用。此外,PFN2 受 miR-494 的负调控。此外,恢复 PFN2 可逆转沉默 SBF2-AS1 对 ESCC 细胞增殖、迁移、侵袭和 EMT 的抑制作用。总之,SBF2-AS1通过海绵状miR-494增强PFN2的表达,从而促进ESCC的细胞增殖、迁移、侵袭和EMT,为ESCC的诊断和治疗提供了有前景的生物标志物。
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来源期刊
Biology Open
Biology Open BIOLOGY-
CiteScore
3.90
自引率
0.00%
发文量
162
审稿时长
8 weeks
期刊介绍: Biology Open (BiO) is an online Open Access journal that publishes peer-reviewed original research across all aspects of the biological sciences. BiO aims to provide rapid publication for scientifically sound observations and valid conclusions, without a requirement for perceived impact.
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Retraction: Overexpression of long non-coding RNA SBF2-AS1 promotes cell progression in esophageal squamous cell carcinoma (ESCC) by repressing miR-494 to up-regulate PFN2 expression. Gene expression and DNA methylation changes in response to hypoxia in toxicant-adapted Atlantic killifish (Fundulus heteroclitus). The Company of Biologists: celebrating 100 years. α-catenin phosphorylation is elevated during mitosis to resist apical rounding and epithelial barrier leak. Air-liquid interface culture combined with differentiation factors reproducing intestinal cell structure formation in vitro.
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