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敲低长链非编码 RNA GHET1 抑制胃癌细胞的激活。

Knockdown of long noncoding RNA GHET1 inhibits cell activation of gastric cancer.

机构信息

Department of Cancer Center, Sichuan Provincial People's Hospital, Chengdu, Sichuian, 610000, China.

Sichuan Cancer Hospital & Institute, Sichuan Cancer Center, School of Medicine, University of Electronic Science and Technology of China, Chengdu, China.

出版信息

Biomed Pharmacother. 2017 Aug;92:562-568. doi: 10.1016/j.biopha.2017.05.088.

DOI:10.1016/j.biopha.2017.05.088
PMID:28577495
Abstract

OBJECTION

The aim of this study was to evaluate the effects of lncRNA GHET1 in developing of Gastric Cancer.

METHODS

Collecting the 20 gastric cancer patients and evaluated the pathological of adjacent and tumor tissues by HE stating. We analyzed the protein expression of Numb in gastric cancer (GC) tissues by using IHC and the gene expression of Numb and GHET1 in adjacent and GC tissues by RT-PCR. The AGS cells were divided into 3 groups: Control (Co), NC and shRNA groups. Measuring the cell proliferation, apoptosis, cell cycle, invasion and migration abilities by MTT, flow cytometry, transwell and wound healing assays. We analyzed the relative signaling pathway by WB assay.

RESULTS

In the clinical analyzing, compared with adjacent tissues, the pathological was significantly changed in tumor tissues, the GHET1 gene and protein expressions were significantly increased in the GC tissues. In the cell experiment, down-regulation of GHET1 had suppressed the cell proliferation, invasion and migration activities and enhanced the cell apoptosis and G1 phase. We found that knockdown of GHET1 dramatically increased E-cadherin, while reducing fibronectin and vimentin.

CONCLUSION

lncRNA GHET1 promoted AGS cells activations, and the results were shown that GHET1 dysregulation might be involved in the occurrence and development of gastric cancer. These results suggested that GHET1 might be a molecular marker for the progression of gastric cancer and a molecular target for targeted therapy.

摘要

异议

本研究旨在评估 lncRNA GHET1 在胃癌发展中的作用。

方法

收集 20 名胃癌患者,通过 HE 染色评估其相邻组织和肿瘤组织的病理变化。采用免疫组化法检测胃癌组织中 Numb 的蛋白表达,采用 RT-PCR 法检测相邻组织和 GC 组织中 Numb 和 GHET1 的基因表达。AGS 细胞分为 3 组:对照组(Co)、阴性对照组(NC)和 shRNA 组。采用 MTT、流式细胞术、Transwell 和划痕愈合实验分别测量细胞增殖、凋亡、细胞周期、侵袭和迁移能力。采用 WB 实验分析相关信号通路。

结果

在临床分析中,与相邻组织相比,肿瘤组织的病理变化明显,GC 组织中的 GHET1 基因和蛋白表达明显增加。在细胞实验中,下调 GHET1 可抑制细胞增殖、侵袭和迁移活性,促进细胞凋亡和 G1 期。我们发现,下调 GHET1 可显著增加 E-钙粘蛋白,同时减少纤连蛋白和波形蛋白。

结论

lncRNA GHET1 促进了 AGS 细胞的激活,结果表明 GHET1 失调可能参与了胃癌的发生和发展。这些结果表明,GHET1 可能是胃癌进展的分子标志物,也是靶向治疗的分子靶点。

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