@Article{096504018X15264647024196,
AUTHOR = {Liping Xue, Bin Lu, Bibo Gao, Yangyang Shi, Jingqi Xu, Rui Yang, Bo Xu, Peng Ding},
TITLE = {NLRP3 Promotes Glioma Cell Proliferation and Invasion  via the Interleukin-1b/NF-kB p65 Signals},
JOURNAL = {Oncology Research},
VOLUME = {27},
YEAR = {2019},
NUMBER = {5},
PAGES = {557--564},
URL = {http://www.techscience.com/or/v27n5/48571},
ISSN = {1555-3906},
ABSTRACT = {Because of the characteristics of high invasiveness, relapse, and poor prognosis, the management of malignant 
gliomas has always been a great challenge. Nod-like receptor (NLR) family pyrin domain containing 3 (NLRP3) is 
a crucial component of the NLRP3 inflammasome, a multiprotein complex that can trigger caspase 1/interleukin-1 
(IL-1)-mediated inflammatory response once activated and participates in the pathogeny of diverse inflammatory 
diseases as well as cancers. We examined the function of NLRP3 in the development of glioma. Glioma cells were 
treated with NLRP3 interference or overexpression vectors, recombinant IL-1 , IL-1 antibody, and NF- B inhibitor. Cell proliferation and invasion were assessed by CCK-8 and Transwell assays. Gene expression was detected 
by PCR, Western blot, and ELISA. NLRP3 and NF- B p65 increased and were positively correlated in glioma 
tissues. NLRP3 knockdown suppressed glioma cell growth and invasion with the decrease of IL-1 and NF- B 
p65. Conversely, forced expression of NLRP3 promoted cell growth. NLRP3 silencing suppressed ectogenous 
IL-1 -elevated cell proliferation and invasion, whereas IL-1 elimination impaired the proproliferation effect of 
NLRP3 hyperexpression. Furthermore, NF- B blockage abrogated IL-1 and NLRP3 hyperexpression increased 
cell growth and invasion. NLRP3 promoted the growth and invasion of gliomas via the IL-1 /NF- B p65 signals.},
DOI = {10.3727/096504018X15264647024196}
}