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E‐cadherin regulates mitochondrial metabolism and induces cell growth through NF‐κB in E‐cadherin deficient AGS cells
Author(s) -
Park Song Yi,
Shin JeeHye,
Kee SunHo
Publication year - 2017
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.31.1_supplement.942.2
Subject(s) - gene knockdown , cadherin , cell growth , microbiology and biotechnology , nf κb , wnt signaling pathway , small hairpin rna , catenin , cancer cell , apoptosis , chemistry , biology , cell , cancer research , signal transduction , cancer , biochemistry , genetics
In this study the interrogation of Wnt regulator β‐catenin and an emerging cancer control molecule NF‐κB was explored in E‐cadherin expressed AGS gastric cancer cells (EC96 cells). It was found that E‐cadherin can increase cell proliferation and energy metabolism through activation of NF‐κB. EC96 cells treated with NF‐κB inhibitors showed a decrease in cell survival. Knockdown of E‐cadherin expression by shRNA could clearly reverse the E‐cadherin‐induced energy metabolism potential in EC96 cells. The application of NF‐kB inhibitors supported the evidence that NF‐kB act as an upstream signal of c‐myc and Glut1. Normally NF‐kB is present in the cytosol of resting cells. Our results showed that E‐cadherin expression led NF‐κB to translocate from cytosol to nucleus in AGS cells. The treatment of NF‐kB inhibitors or knockdown with E‐cadherin shRNA abolished the ability of E‐cadherin to translocate NF‐kB into nucleus in EC96 cells, which was accompanied with the reduction of cell growth. In conclusion, E‐cadherin expression generates cell proliferation signals through NF‐κB signal pathway as Wnt signal pathway was suppressed. Support or Funding Information [This research was supported by Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Education (NRF‐2015R1D1A1A09056775)]