Open AccessResistin facilitates metastasis of lung adenocarcinoma through the TLR 4/Src/ EGFR / PI 3K/ NF ‐κB pathway
Author(s) -
Gong WeiJing,
Liu JunYan,
Yin JiYe,
Cui JiaJia,
Xiao Di,
Zhuo Wei,
Luo Chao,
Liu RuiJie,
Li Xi,
Zhang Wei,
Zhou HongHao,
Liu ZhaoQian
Publication year - 2018
Publication title -
cancer science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.035
H-Index - 141
eISSN - 1349-7006
pISSN - 1347-9032
DOI - 10.1111/cas.13704
Subject(s) - resistin , metastasis , cancer research , adenocarcinoma , epidermal growth factor receptor , receptor , tumor microenvironment , a549 cell , medicine , lung cancer , biology , cancer , leptin , adipokine , obesity
Metastasis is the main cause of lung cancer‐related death. The tumor microenvironment greatly contributes to tumor metastasis. Resistin, mainly secreted by tumor‐associated macrophages in tumor tissues, is a 12.5‐kDa cysteine‐rich secretory protein that is found at significantly higher levels in the serum or plasma of cancer patients compared with healthy controls. In this study, we explored the expression and role of resistin in lung adenocarcinoma. Our study showed that resistin was strongly expressed in lung adenocarcinoma tissues and promoted the migration and invasion of lung adenocarcinoma cells in a dose‐dependent manner. Toll‐like receptor 4 ( TLR 4) was the functional receptor of resistin for migration and invasion in A549 cells. Src/epidermal growth factor receptor ( EGFR ) was involved in resistin‐induced migration and invasion. Resistin increased the phosphorylation of EGFR through the TLR 4/Src pathway. We also found that PI 3K/nuclear factor (NF)‐κB were the intracellular downstream effectors mediating resistin‐induced migration and invasion. Taken together, our results suggested that resistin promoted lung adenocarcinoma metastasis through the TLR 4/Src/ EGFR / PI 3K/ NF ‐κB pathway.