The results revealed that exRNAs from lung cancer CCS promoted the inflammatory cytokine interleukin‑1β and reduced the vascular cell adhesion molecule‑1 expression in lung epithelial cells.
Here, we further showed that lung cancer microparticles (L-MPs) induce macrophages to release a key proinflammatory cytokine, IL-1β, thus promoting lung cancer development.
This review will summarize the role of inflammation in cancer propagation and development, discuss the biological rationale for targeting interleukin-1β in lung cancer, advocate for further investigation of the anti-inflammatory antibody canakinumab as a new attractive mechanism for future lung cancer therapy, and discuss future and ongoing trials.
In this study, almost all saponins with oleanolic acid as aglycones exhibited significant hemolysis, monodesmosidic saponins with hederagenin as aglycone were the most active compounds against lung cancer cells with greater activity than standard commercial chemotherapy drug doxorubicin and some of the hederagenin type saponins induced remarkable IL-1β secretion.
Our hypothesis-generating data suggest the possibility that anti-inflammatory therapy with canakinumab targeting the interleukin-1β innate immunity pathway could significantly reduce incident lung cancer and lung cancer mortality.
In addition, analysis of breast and lung cancer patient cohorts demonstrated that interaction between p73 and IL-1β predicts a negative survival outcome in these human cancers.
PBMC gene expression of CCL3, IL8 and IL1β was higher in lung cancer patients compared to the same patients at each of four sequential timepoints after removal of their tumors, while CXCL10 and IL2Rα were essentially unchanged.
Lung cancer risk also increased with the number of polymorphism sites where at least 1 'risk' allele was present [interleukin 1-β-31T/C (T allele), IL1RN (*2 allele) and IL6-634C/G (G allele)] among those with asthma, cough or atopy (Ptrend 0.001) but not in those without (Ptrend 0.47).
Our findings indicate the possible association of the T allele carriers of the IL1Brs1143634 polymorphism with higher risk of lung cancer especially among smokers.
Various single-nucleotide polymorphisms (SNPs) in apoptotic genes have been associated with increased risks in lung cancer, particularly FAS -1377 G>A (rs2234767), FASLG -844 C>T (rs763110), IL1B +3954 C>T Phe105Phe (rs1143634) and BAT3 Ser625Pro (rs1052486).
A global test of association for 42 SNPs, which excluded eight SNPs that were in very tight linkage disequilibrium with other SNPs, was statistically significant (P = 0.01), suggesting that overall genetic variation in this pathway contributes to lung cancer risk.In addition, the IL1B -1060TT (i.e.
The antiproliferative effect of trans-retinoic acid is associated with selective induction of interleukin-1 beta, a cytokine that directly inhibits growth of lung cancer cells.