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LETM1 Promotes Gastric Cancer Cell Proliferation, Migration, and Invasion via the PI3K/Akt Signaling Pathway
Journal of Gastric Cancer ( IF 3.2 ) Pub Date : 2020-01-01 , DOI: 10.5230/jgc.2020.20.e12
Yunfeng Zhang 1 , Lele Chen 1 , Yifan Cao 1 , Si Chen 1 , Chao Xu 1 , Jun Xing 1 , Kaiguang Zhang 1
Affiliation  

Purpose Globally, there is a high incidence of gastric cancer (GC). Leucine zipper-EF-hand containing transmembrane protein 1 (LETM1) is reported to play a vital role in several human malignancies. However, there is limited understanding of the role of LETM1 in GC. This study aims to investigate the effects of LETM1 on proliferation, migration, and invasion of GC cells. Materials and Methods The expression levels of LETM1 in the normal gastric mucosal epithelial cells (GES-1) and GC cells were analyzed by quantitative real-time polymerase chain reaction and western blotting. CCK-8, wound healing, and Transwell invasion assays were performed to evaluate the effect of LETM1 knockdown or overexpression on the proliferation, migration, and invasion of the GC cells, respectively. Additionally, the effect of LETM1 knockdown or overexpression on GC cell apoptosis was determined by flow cytometry. Furthermore, the effect of LETM1 knockdown or overexpression on the expression levels of PI3K/Akt signaling pathway-related proteins was evaluated by western blotting. Results The GC cells exhibited markedly higher mRNA and protein expression levels of LETM1 than the GES-1 cells. Additionally, the knockdown of LETM1 remarkably suppressed the GC cell proliferation, migration, and invasion, and promoted the apoptosis of GC cells, which were reversed upon LETM1 overexpression. Furthermore, the western blotting analysis indicated that LETM1 facilitates GC progression via the PI3K/Akt signaling pathway. Conclusions LETM1 acts as an oncogenic gene to promote GC cell proliferation, migration, and invasion via the PI3K/Akt signaling pathway. Therefore, LETM1 may be a potential target for GC diagnosis and treatment.

中文翻译:

LETM1通过PI3K/Akt信号通路促进胃癌细胞增殖、迁移和侵袭

目的 在全球范围内,胃癌 (GC) 的发病率很高。据报道,含有跨膜蛋白 1 (LETM1) 的亮氨酸拉链-EF-手在几种人类恶性肿瘤中起着至关重要的作用。然而,对 LETM1 在 GC 中的作用了解有限。本研究旨在研究 LETM1 对 GC 细胞增殖、迁移和侵袭的影响。材料与方法通过定量实时聚合酶链反应和蛋白质印迹分析LETM1在正常胃黏膜上皮细胞(GES-1)和GC细胞中的表达水平。进行 CCK-8、伤口愈合和 Transwell 侵袭试验以分别评估 LETM1 敲低或过表达对 GC 细胞增殖、迁移和侵袭的影响。此外,通过流式细胞术确定 LETM1 敲低或过表达对 GC 细胞凋亡的影响。此外,通过蛋白质印迹评估 LETM1 敲低或过表达对 PI3K/Akt 信号通路相关蛋白表达水平的影响。结果GC细胞LETM1的mRNA和蛋白表达水平明显高于GES-1细胞。此外,敲低 LETM1 显着抑制了 GC 细胞的增殖、迁移和侵袭,并促进了 GC 细胞的凋亡,这些在 LETM1 过表达后被逆转。此外,蛋白质印迹分析表明 LETM1 通过 PI3K/Akt 信号通路促进 GC 进展。结论 LETM1作为致癌基因通过PI3K/Akt信号通路促进GC细胞增殖、迁移和侵袭。所以,
更新日期:2020-01-01
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