Lung cancer is the leading cause of cancer death, and it is widely accepted that 
chronic inflammation is an important risk for the development of lung cancer. 
Now, it is recognized that the nucleotide-binding and oligomerization domain 
(NOD) like receptors (NLRs)-containing inflammasomes are involved in 
cancer-related inflammation. This study was designed to investigate the effects 
of NLR family pyrin domain containing protein 3 (NLRP3) inflammasome on the 
proliferation and migration of lung adenocarcinoma cell line A549. Using 
5-ethynyl-2'-deoxyuridine (EdU) incorporation assay, scratch assay, and 
Transwell migration assay, we showed that activation of the NLRP3 inflammasome 
by LPS+ATP enhanced the proliferation and migration of A549 cells. Western blot 
analysis showed that activation of phosphorylation of Akt, ERK1/2, CREB and the 
expression of Snail increased, while the expression of E-cadherin decreased 
after the activation of NLRP3 inflammasome. Moreover, these effects were 
inhibited by the following treatments: i) downregulating the expression of NLRP3 
by short hairpin RNA (shRNA) interference, ii) inhibiting the activation of 
NLRP3 inflammasome with a caspase-1 inhibitor, iii) blocking the interleukin-1β 
(IL-1β) and IL-18 signal transduction with IL-1 receptor antagonist (IL-1Ra) and 
IL-18 binding protein (IL-18BP). Collectively, these results indicate that NLRP3 
inflammasome plays a vital role in regulating the proliferation and migration of 
A549 cells and it might be a potential target for the treatment of lung cancer.