lncRNA SNHG14在胃癌中的作用:增强肿瘤细胞的增殖和迁移以及CDH2的表达机制。

IF 3.4 3区 生物学 Q3 CELL BIOLOGY
Cell Cycle Pub Date : 2023-12-01 Epub Date: 2024-01-09 DOI:10.1080/15384101.2023.2289745
Zhou-Tong Dai, Yong-Lin Wu, Tao Xu, Xing-Rui Li, Teng Ji
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引用次数: 0

摘要

LncRNA 是一类非编码 RNA,在调控基因表达方面发挥着重要作用。然而,它们在胃癌发生和转移中的具体分子机制还需要进一步探索。TCGA数据显示,与生存密切相关的MFGE8的表达与lncRNA SNHG14呈显著正相关。此外,高通量测序和 qRT-PCR 结果表明,lncRNA SNHG14 在胃癌中明显升高。此外,体外功能实现表明,lncRNA SNHG14的过表达会明显增加胃癌的增殖、侵袭和迁移。动物实验也表明,lncRNA SNHG14的过表达促进了体内肿瘤的发生和转移。从机理上讲,MFGE8可激活lncRNA SNHG14的表达,而SNHG14可通过稳定CDH2激活细胞的EMT。我们的研究表明,lncRNA SNHG14可能是胃癌治疗的潜在靶点。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The role of lncRNA SNHG14 in gastric cancer: enhancing tumor cell proliferation and migration, and mechanisms of CDH2 expression.

LncRNAs are a class of non-coding RNAs that play an important role in regulating gene expression. However, their specific molecular mechanisms in gastric carcinogenesis and metastasis need further exploration. TCGA data showed that the expression of MFGE8, which was closely related to survival, was significantly positively correlated with lncRNA SNHG14. And moreover, the results of high-throughput sequencing and qRT-PCR showed that lncRNA SNHG14 was significantly elevated in gastric cancer. Further, in vitro functional realization showed that lncRNA SNHG14 overexpression significantly increased gastric cancer's proliferation, invasion and migration. Animal experiments also showed that lncRNA SNHG14 overexpression promoted tumorigenesis and metastasis in vivo. Mechanistically, MFGE8 activates the expression of lncRNA SNHG14, which activates the cellular EMT by stabilizing CDH2. Our study suggests that lncRNA SNHG14 could be a potential target for gastric cancer therapy.

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来源期刊
Cell Cycle
Cell Cycle 生物-细胞生物学
CiteScore
7.70
自引率
2.30%
发文量
281
审稿时长
1 months
期刊介绍: Cell Cycle is a bi-weekly peer-reviewed journal of high priority research from all areas of cell biology. Cell Cycle covers all topics from yeast to man, from DNA to function, from development to aging, from stem cells to cell senescence, from metabolism to cell death, from cancer to neurobiology, from molecular biology to therapeutics. Our goal is fast publication of outstanding research.
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