LINC02266通过调控AKT/ACSL4通路促进胃癌细胞增殖转移,抑制铁下垂。

IF 3.7 2区 生物学 Q3 CELL BIOLOGY
Xiaoru Liang, Xinyu Niu, Lijie Zhang, Chang Liu, Xiaomin Zhao, Feng Chen, Zhijuan Lin
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引用次数: 0

摘要

铁死亡是一种以铁依赖性氧化损伤、脂质过氧化和活性氧积累为特征的新型细胞死亡形式。铁下垂与胃癌(GC)有密切关系。最近的研究表明,许多与嗜铁性凋亡相关的长链非编码rna (lncRNAs)影响GC的发生和进展。然而,确切的机制尚未阐明。本研究表明,一种新型lncRNA LINC02266在胃癌细胞中表达上调,是与胃癌预后和进展相关的关键lncRNA。功能分析表明,LINC02266抑制铁下垂,促进GC细胞的增殖、迁移、侵袭和肿瘤生长。在机制上,我们发现LINC02266通过抑制ACSL4水平抑制erastin诱导的铁下垂,这可能与AKT通路有关。本研究提示LINC02266可作为胃癌的诊断标志物和新的治疗靶点。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
LINC02266 promotes proliferation and metastasis and inhibits ferroptosis of gastric cancer cells by regulating AKT/ACSL4 pathway.

Ferroptosis is a novel form of cell death characterized by iron-dependent oxidative damage, lipid peroxidation, and the accumulation of reactive oxygen species. There exists a close correlation between ferroptosis and gastric cancer (GC). Recent research has shown that many ferroptosis-related long non-coding RNAs (lncRNAs) affect the occurrence and progression of GC. However, the exact mechanism has not been elucidated. This study showed that a novel lncRNA LINC02266 was upregulated in GC cells and was a key lncRNA associated with GC prognosis and progression. Functional analysis indicated that LINC02266 suppressed ferroptosis and promoted GC cell proliferation, migration, invasion, and tumor growth in vitro and vivo. Mechanistically, we found that LINC02266 inhibited erastin-induced ferroptosis by suppressing ACSL4 levels, which may be related to the AKT pathway. This study indicates that LINC02266 can serve as a diagnostic marker and novel therapeutic target for GC.

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来源期刊
Molecular and Cellular Biochemistry
Molecular and Cellular Biochemistry 生物-细胞生物学
CiteScore
8.30
自引率
2.30%
发文量
293
审稿时长
1.7 months
期刊介绍: Molecular and Cellular Biochemistry: An International Journal for Chemical Biology in Health and Disease publishes original research papers and short communications in all areas of the biochemical sciences, emphasizing novel findings relevant to the biochemical basis of cellular function and disease processes, as well as the mechanics of action of hormones and chemical agents. Coverage includes membrane transport, receptor mechanism, immune response, secretory processes, and cytoskeletal function, as well as biochemical structure-function relationships in the cell. In addition to the reports of original research, the journal publishes state of the art reviews. Specific subjects covered by Molecular and Cellular Biochemistry include cellular metabolism, cellular pathophysiology, enzymology, ion transport, lipid biochemistry, membrane biochemistry, molecular biology, nuclear structure and function, and protein chemistry.
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