Genetic deletion of the IL-1 receptor (IL-1R1) in epithelial cells alleviated tumorigenesis in the APC model of CRC, demonstrating a cell-autonomous role for IL-1 signaling in early tumor seed outgrowth.
The administration of BL to CRC-mice resulted in a dramatic increase in IL-1β mRNA and IL-1β concentration, which in contrast was accompanied with a decrease in the IL-6 mRNA and IL-6 concentration.
These results lead to a conclusion that modulation of IL-1 receptor activity could have applications as a part of combination therapy for advanced and highly metastatic colorectal cancers.
We studied the effect of heat-killed cells of <i>E. faecalis</i> on NLRP3 inflammasome activation in THP-1-derived macrophages.Pretreatment of <i>E. faecalis</i> or NLRP3 siRNA can inhibit NLRP3 inflammasome activation in macrophages in response to fecal content or commensal microbes, <i>P. mirabilis</i> or <i>E. coli</i>, according to the reduction of caspase-1 activation and IL-1β maturation.Mechanistically, <i>E. faecalis</i> attenuates the phagocytosis that is required for the full activation of the NLRP3 inflammasome.In in vivo mouse experiments, <i>E. faecalis</i> can ameliorate the severity of intestinal inflammation and thereby protect mice from dextran sodium sulfate (DSS)-induced colitis and the formation of CRC in wild type mice.On the other hand, <i>E. faecalis</i> cannot prevent DSS-induced colitis in NLRP3 knockout mice.
Knockdown of ZEB1 in CRC cells inhibited 8-oxo-dG induction by oxidative stress (H<sub>2</sub>O<sub>2</sub>) and inflammatory cytokines (interleukin (IL)1β).
Moreover, TNFSF9 and IL-1β expression was significantly increased in human CRCs when compared to normal colon (P < 0.05), and was associated with AI-2 concentration and increased survival.
Accumulating scientific evidence has revealed that interleukin (IL)-33, an IL-1 family member, plays an essential role in the regulation of immune response and is relevant in CRC pathogenesis.
Mechanical exploration revealed that TRIM31 mediated the upregulation of inflammatory cytokines TNF, IL-1β, and IL-6 through the NF-κB pathway, thus contributing to EMT in CRC progression.
Other studies have found that mutation of rs1143627 of IL1B (allelic model: OR 2.97; 95% CI 1.74-5.05, P < 0.001) and rs1050152 of OCTN1 (allelic model: OR 1.637, 95% CI 1.078-2.485, P = 0.021) increased the proportion of IBD-associated CRC in the population.
We conclude that Colombian individuals with high African ancestry proportions at locus 2q14 harbour more IL1B-CGTC copies and are consequently at an increased risk of CRC.
These data provide insight into the metabolic effects induced by IL-1β in colorectal cancer, and identify relevant targets that may be exploited to block the effects of this cytokine..
Here we reported that LPS treatment increased PKM expression through activation of NF-κB signalling pathway, and knockdown of PKM reversed LPS-induced TNF-α, IL-1β production and cell proliferation in CRC cells.
The study aimed to assess whether polymorphisms in ABCB1, ABCC2 and ABCG2 were associated with risk of colorectal cancer (CRC) and to investigate gene-environment (dietary factors, smoking and use of non-steroidal anti-inflammatory drugs) and gene-gene interactions between previously studied polymorphisms in IL1B and IL10 and ABC transporter genes in relation to CRC risk.
Our results, combined with previous studies, suggest that IL10, PSCA, IL1B, and SMAD7 are significantly correlated with CRC susceptibility in the Han Chinese population.
Accordingly, IL1β and IL23 genes, typically expressed by M1 macrophages, were expressed to significantly (P < 0.001) higher extents in colorectal cancer than in healthy mucosa.
A case-control study of 401 cases and 300 sex- and age-matched controls was performed in order to explore the role of IL1B_1473G/C (rs1143623), SOD1_7958A/G (rs4998557), TLR4_1196C/T (rs4986791), IL10_1082A/G (rs1800896), IL17A_197G/A (rs2275913), and TLR4_896A/G (rs4986790) polymorphisms in the susceptibility to colorectal cancer (n = 244), gastric carcinoma (n = 72), and ovarian cancer (n = 85).
The current study indicated that colorectal cancer is remarkably associated with SGMB; moreover, molecular detection of SGMB in CRC was superior to link SGMB with CRC tumors highlighting a possible direct and active role of SGMB in CRC development through most probably inflammation-based sequel of tumor development or propagation via, but not limited to, IL-1, COX-2, and IL-8.
The authors assessed polymorphisms of the interleukin: IL-1, IL-1R, IL-2, IL-4, IL-4R, IL-10, transforming growth factor (TGF)-β1, IFN-γ genes in Korean patients with colorectal cancer (n = 170) and in a normal healthy control group (n = 130) to investigate the association between theses cytokine gene polymorphisms and the risk of colorectal cancer.
We examined association between IL-1 locus polymorphisms and risk of esophageal, gastric and colorectal carcinomas in Japanese patients with H. pylori infection.