In this study, we aim to evaluate Toll-like receptor 2 (TLR2) expression in human glioma tumors and the correlation between its expression with degrees of malignancy and autophagy, development of tumors.
The available evidence indicates that curcumin inhibits the extracellular TLR 2 and 4 and intracellular TLR9 and thereby exerts a therapeutic effect in diseases such as cancer, inflammation, infection, autoimmune, and ischemic disease.
We used STATA to calculate the odds ratio (OR) and 95% confidence interval (95% CI) to evaluate the relationship between certain polymorphism of TLR2 and cancer risk.
The transcriptome signature of colon cancer-cocultured MCs may potentially reflect the mechanism of how colon cancer cells educate MCs to become pro-tumorigenic in the initial phase and how a subsequent inflammatory signal-e.g., TLR2 ligands-may modify their responses in the cancer milieu.
Serum levels of TLR ligands, the prevalence of malignancy-associated abnormal activated/germinal center-like (CD19CD10CD71CD86AID) B cells, TLR2 expression on B cells, expression of TLR2-modulating micro-RNA, and the frequency of regulatory T and B cells were assessed.
In stratified analysis, we found the effect of TLR2 -196 to -174 del on cancer risk remained significant in the subgroup of Caucasians and South Asians, but not in East Asians.
The present meta-analysis suggests that TLR2+597T>C (rs3804099), +1350C>T (rs3804100) and rs5743708" genes_norm="7097">Arg753Gln (rs5743708) polymorphisms are not associated with cancer risk.
Our meta-analysis identified that elevated cancer risk was statistically associated with -196 to -174 del allele in -196 to -174 del polymorphism (OR=1.63, 95% CI=1.10-2.41 for allele comparison; OR=1.64, 95% CI=1.05-2.57 for dominant model; OR=2.26, 95% CI=1.24-4.12 for recessive model; OR=2.57, 95% CI=1.30-5.08 for DD vs. II and OR=1.53, 95% CI=1.01-2.32 for ID vs. II in codominant model); whereas rs3804099 in TLR-2 was associated with decreased cancer risk.
In conclusion, the Delta22 and rs3804100 polymorphisms in TLR2 are risk factors for cancer susceptibility while the TLR2rs3804099 dominant genotype is a protective factor, especially in Asians.
This TLR-specific difference in expression suggested that such expression does not only reflect a local inflammatory response to cancer infiltration, i.e., if this was the case, both TLR2 and 4 expression would probably be up-regulated.
However, the frequency of TLR2 -196 to -174 ins/del + del/del and TLR4+896AG genotypes was significantly higher (P < 0.01 and P = 0.01, respectively) in the cancer group (33.4% and 11.5%, respectively) than in the control group (16.9% and 4.5%, respectively).
TLR2 in MDA-MB-231 cells were actively triggered by peptidoglycan (PGN) from infectious bacterium Staphylococcus aureus (PGN-SA), resulting in the promoted invasiveness and adhesiveness of the cancer cells in vitro.
Putative biomarkers such as cell cycle related genes (Cdc37), cancer cell adhesion (Glycam 1, integrin alpha8, integrin alphaX and Clec4n), signal transduction (Tlr2, IL-33, and Ccbp2), migration (Ccr1, Ccl6, and diaphorase 1 (Cyb5r3) and cancer development (epiregulin) can be useful for diagnosis and as prognosis markers and some of the target molecules can be applied for prevention of cancer.
An analysis of all per cent variability values with regard to malignancy stage increasing from polyp to stages I to III adenocarcinoma, and normal colon mucosa shows a statistically significant relationship for TLR2 (increasing) and TLR3 (decreasing).
In this study, we report that H. pylori-induced COX-2 expression enhances the cancer cell invasion and angiogenesis via TLR2 and TLR9, which can be attenuated by the specific COX-2 inhibitor NS398 or celecoxib.