Akademik Veri Yönetim Sistemi
JOURNAL OF GASTROINTESTINAL CANCER, cilt.54, sa.1, ss.227-236, 2023 (ESCI, Scopus)
In this review, we aimed to elaborate on these findings and explore how NLRP3 inflammasome affects CRC and which mechanism could be a potential therapeutic target. For this purpose, major indexing databases consist of Cochrane central, ISI web of science (WOS), PubMed/Medline, Scopus, and EMBASE were systematically searched using standard terms without any language, study region, or type restrictions. After applying the exclusion criteria, the main properties of 12 articles on 326 animals included in this meta-analysis. Of 12, eight were about an anti-tumoral effect, and four were on a pro-tumoral effect of the inflammasome. NLRP3 inhibition reduced IL-1 beta (SMD: -4.14, 95% CI: -5.49, -2.79, P < 0.00001, I-2 = 76%), TNF alpha (SMD: -2.18, 95% CI: -3.23, -1.13, P < 0.00001, I-2 = 82%), and IL-18 (SMD: -2.27, 95% CI: -3.38, -1.16, P = 0.0002, I-2 = 74%) significantly contrasted with the model controls. Colons harvested from NLRP3 inhibition groups showed significant truncation compared with the model controls (SMD: -1.75, 95% CI: -2.69, -0.81, P = 0.0003, I-2 = 60%). We demonstrated significantly decreased tumorigenesis following NLRP3 inactivation, as well as an increased survival rate compared with the model controls. To translate anti-cancer agents based on anti-NLRP3 from bench to bedside, it is necessary to identify the molecules that selectively target NLRP3 or its downstream pathways in malignant cells, as well as considering metabolic heterogeneity and the mechanisms causing such cancer-connected heterogeneity. Other studies are needed to separate the molecular and functional complexity of this network.