The influence of LRRC3B on esophageal cancer cell Eca109 migration, invasion and PI3K/Akt signaling pathway

曹燕飞; 任　睿; 杨　晔

doi:10.19401/j.cnki.1007-3639.2017.05.005

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The influence of LRRC3B on esophageal cancer cell Eca109 migration, invasion and PI3K/Akt signaling pathway

更新时间：2025-12-31

- The influence of LRRC3B on esophageal cancer cell Eca109 migration, invasion and PI3K/Akt signaling pathway
- China Oncology Vol. 27, Issue 5, Pages: 345-352(2017)
- 作者机构：
  
  1. 陕西省人民医院胸外科,陕西,西安,710068
  2. 陕西省新安中心医院妇产科,陕西,西安,710048
- 作者简介：
- 基金信息：
- DOI：10.19401/j.cnki.1007-3639.2017.05.005
  CLC：
- Published Online：14 June 2017，
  
  Published：14 June 2017
- 稿件说明：
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曹燕飞,任　睿,杨　晔,等. LRRC3B对食管癌细胞Eca109迁移、侵袭及PI3K/Akt信号通路的影响[J]. 中国癌症杂志, 2017, 27(5): 345-352.

曹燕飞, 任　睿, 杨　晔. The influence of LRRC3B on esophageal cancer cell Eca109 migration, invasion and PI3K/Akt signaling pathway[J]. China Oncology, 2017, 27(5): 345-352.
曹燕飞,任　睿,杨　晔,等. LRRC3B对食管癌细胞Eca109迁移、侵袭及PI3K/Akt信号通路的影响[J]. 中国癌症杂志, 2017, 27(5): 345-352. DOI： 10.19401/j.cnki.1007-3639.2017.05.005.

曹燕飞, 任　睿, 杨　晔. The influence of LRRC3B on esophageal cancer cell Eca109 migration, invasion and PI3K/Akt signaling pathway[J]. China Oncology, 2017, 27(5): 345-352. DOI： 10.19401/j.cnki.1007-3639.2017.05.005.

摘要

背景与目的：先前的研究已经证实富含亮氨酸重复序列3B蛋白(leucine-rich repeatcontaining 3B，LRRC3B)在多种癌症中低表达，并且与癌细胞的迁移侵袭密切相关。该研究旨在探讨LRRC3B在食管癌发展中的作用机制。方法：免疫组织化学染色检测LRRC3B在60例食管癌组织及60例癌旁组织中的表达情况，采用实时荧光定量聚合酶链反应(real-time fluorescent quantitative polymerase chain reaction，RTFQ-PCR)和蛋白[质]印迹法(Western blot)分别检测食管癌细胞Eca109和食管正常上皮细胞系HEEC中LRRC3B的mRNA和蛋白表达。处理食管癌细胞Eca109并分3组：正常对照组、阴性对照组(转染对照空pCMV6质粒)和过表达LRRC3B组(转染pCMV6-LRRC3B过表达质粒)。采用Transwell法检测各组Eca109细胞迁移和侵袭的变化。采用Western blot检测各组细胞中上皮间质转化(epithelial-mesenchymal transition，EMT)相关蛋白E-cadherin、N-cadherin和Vimentin表达以及p-Akt蛋白水平。结果：LRRC3B在食管癌组织和细胞中的表达明显低于癌旁组织和食管正常上皮细胞。过表达LRRC3B明显抑制Eca109细胞的迁移和侵袭能力，上调上皮因子E-cadherin表达，抑制间质标志物N-cadherin和Vimentin表达，同时降低细胞内p-Akt水平。结论：LRRC3B在食管癌中低表达，上调LRRC3B能够抑制食管癌细胞的EMT过程，可能与抑制PI3K/Akt信号通路有关。

Abstract

Background and purpose: Previous studies have confirmed that the expression of leucine-rich repeat-containing 3B (CLRRC3B) was significantly decreased in different human cancers

which was also associated with the migration and invasion of cancer cells. The aim of this study was to explore the potential mechanism of LRRC3B in the development of esophageal cancer. Methods: The LRRC3B expression was detected in 60 cancer tissues and 60 adjacent non-neoplastic tissues by immunohistochemistry. The mRNA and protein expression of LRRC3B in Eca109 and HEECs were detected using real-time fluorescence quantitative polymerase chain reaction (RTFQ-PCR) and Western blot

respectively. Eca109 cells with different treatments were divided into three groups: normal group

negative control group (transfected with pCMV6 plasmid)

overexpression LRRC3B group (transfected with pCMV6-LRRC3B plasmid). Transwell assay was used to measure the migration and invasion of Eca109 cells in different groups. The protein levels of E-cadherin

N-cadherin

Vimentin and p-Akt were determined by Western blot. Results: The expression of LRRC3B in esophageal cancer tissues was lower than that of non-cancerous tissues

as well as the expression of LRRC3B in Eca109 was decreased compared with that of normal esophageal epithelial cell line HEEC. Overexpression of LRRC3B significantly inhibited Eca109 cells migration and invasion

upregulated the expression of E-cadherin and decreased the expression of N-cadherin and Vimentin. Moreover

overexpression of LRRC3B significantly inhibited the phosphorylation of Akt in Eca109 cells. Conclusion: The expression of LRRC3B was decreased in esophageal cancer. Overexpression of LRRC3B can efficiently inhibit the EMT progression in esophageal cancer cells by suppressing PI3K/Akt signaling pathway.

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