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长链非编码 RNA ZFAS1 通过体外 PI3K/AKT 通路促进鼻咽癌细胞增殖、迁移和抑制凋亡。

LncRNA ZFAS1 promotes proliferation and migration and inhibits apoptosis in nasopharyngeal carcinoma via the PI3K/AKT pathway in vitro.

机构信息

The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, China.

Taizhou Minicipal Hospital, Taizhou, Zhejiang, China.

出版信息

Cancer Biomark. 2019;26(2):171-182. doi: 10.3233/CBM-182080.

DOI:10.3233/CBM-182080
PMID:31403940
Abstract

BACKGROUND

Increasing evidence shows that long non-coding RNAs (lncRNAs) play a key role in the development of various cancers. Zinc finger antisense 1 (ZFAS1) is a novel lncRNA with previously demonstrated associations with several types of cancer. Here we examined the expression and potential function of the ZFAS1 in nasopharyngeal carcinoma (NPC).

METHODS

We detected ZFAS1 expression in GSE12452, a human microarray dataset, and NPC cell lines. Small interfering RNA against ZFAS1 was used to elucidate the cellular functions of ZFAS1 using MTT, colony formation, cell cycle, cell apoptosis, transwell invasion and migration and western blot assays. An activator of the PI3K/AKT signaling pathway (740Y-P) was used to determine the contribution of PI3K/AKT.

RESULTS

ZFAS1 was significantly upregulated in NPC tissues and cell lines. Silencing ZFAS1 significantly inhibited cell proliferation and invasion, arrested cell cycle progression and promoted cell apoptosis, as well as reduced epithelial-mesenchymal transition. Moreover, 740Y-P could rescue the effects of ZFAS1 knockdown on proliferation, apoptosis and invasion in 5-8F cells.

CONCLUSIONS

ZFAS1 might play an oncogenic role in NPC and facilitate cell proliferation and invasion via the PI3K/AKT signaling pathway in NPC cells.

摘要

背景

越来越多的证据表明,长非编码 RNA(lncRNA)在各种癌症的发展中起着关键作用。锌指反义 1(ZFAS1)是一种新型的 lncRNA,先前已证明其与几种类型的癌症有关。在这里,我们研究了 ZFAS1 在鼻咽癌(NPC)中的表达和潜在功能。

方法

我们在 GSE12452 人类微阵列数据集和 NPC 细胞系中检测了 ZFAS1 的表达。使用针对 ZFAS1 的小干扰 RNA 来阐明 ZFAS1 的细胞功能,使用 MTT、集落形成、细胞周期、细胞凋亡、Transwell 侵袭和迁移以及 Western blot 分析。使用 PI3K/AKT 信号通路的激活剂(740Y-P)来确定 PI3K/AKT 的贡献。

结果

ZFAS1 在 NPC 组织和细胞系中显著上调。沉默 ZFAS1 可显著抑制细胞增殖和侵袭,阻滞细胞周期进程并促进细胞凋亡,并减少上皮-间充质转化。此外,740Y-P 可挽救 5-8F 细胞中 ZFAS1 敲低对增殖、凋亡和侵袭的影响。

结论

ZFAS1 可能在 NPC 中发挥致癌作用,并通过 NPC 细胞中的 PI3K/AKT 信号通路促进细胞增殖和侵袭。

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