Department of Gastrointestinal Surgery, Jining No. 1 People's Hospital, Jining, Shandong, China.
Eur Rev Med Pharmacol Sci. 2018 Jul;22(13):4128-4137. doi: 10.26355/eurrev_201807_15405.
Gastric carcinoma (GC) is a common cancer with heavy mortality and poor outcome at advanced stages and metastasis. Long non-coding RNA nuclear-enriched abundant transcript 1 (NEAT1) has been reported to be an oncogene in GC recently. However, the underlying mechanism is far from understood. We aimed to explore the role of NEAT1 in GC as well as the underlying mechanisms.
The expression of NEAT1 in clinical human GC tissues and GC cell lines were assessed by quantitative reverse transcription PCR. Then, NEAT1 was non-physiologically expressed in GC cells (SGC-7901 and MKN45 cells), followed by estimation of cell viability, migration, invasion, apoptosis, activation of the phosphatidylinositol-3-kinase (PI3K)/AKT and glycogen synthase kinase 3β (GSK3β) pathways, and microRNA (miR)-17 level. Moreover, the effects of miR-17 inhibition on cell viability, migration, and activation of the PI3K/AKT and GSK3β pathways in GC cells overexpressing NEAT1 were also explored.
NEAT1 was up-regulated in GC tissues and cell lines. Then, cell viability and migration of GC cells were markedly increased by NEAT1 overexpression, while the cell invasion and apoptosis were unchanged. The phosphorylated level of PI3K, AKT, and GSK3β were increased by NEAT1 overexpression. Subsequently, we found miR-17 level was positively correlated with NEAT1 expression, and NEAT1 functions through up-regulating miR-17.
NEAT1 was up-regulated in GC tissues and cell lines. Its overexpression enhanced cell viability and migration through up-regulating miR-17, along with activation of the PI3K/AKT and GSK3β pathways.
胃癌（GC）是一种常见的癌症，其死亡率高，晚期和转移阶段的预后较差。长链非编码 RNA 核富集丰富转录本 1（NEAT1）最近被报道为 GC 的癌基因。然而，其潜在机制还远未被理解。我们旨在探讨 NEAT1 在 GC 中的作用及其潜在机制。
通过定量逆转录 PCR 评估临床人 GC 组织和 GC 细胞系中 NEAT1 的表达。然后，在 GC 细胞（SGC-7901 和 MKN45 细胞）中非生理表达 NEAT1，随后评估细胞活力、迁移、侵袭、凋亡、磷脂酰肌醇-3-激酶（PI3K）/AKT 和糖原合酶激酶 3β（GSK3β）途径的激活以及 microRNA（miR）-17 水平。此外，还探讨了 miR-17 抑制对过表达 NEAT1 的 GC 细胞活力、迁移和 PI3K/AKT 和 GSK3β 途径激活的影响。
NEAT1 在 GC 组织和细胞系中上调。然后，NEAT1 的过表达显著增加了 GC 细胞的活力和迁移，而细胞侵袭和凋亡没有改变。PI3K、AKT 和 GSK3β 的磷酸化水平因 NEAT1 的过表达而增加。随后，我们发现 miR-17 水平与 NEAT1 表达呈正相关，NEAT1 通过上调 miR-17 发挥作用。
NEAT1 在 GC 组织和细胞系中上调。其过表达通过上调 miR-17 增强细胞活力和迁移，同时激活 PI3K/AKT 和 GSK3β 途径。
