AI Article Synopsis
- Colorectal cancer (CRC) is the leading cause of cancer-related deaths worldwide, and research suggests a link between the NLRP3 protein and the disease's growth and spread.
- Various laboratory methods, including qPCR and animal studies, showed that higher NLRP3 levels in CRC tissues corresponded with worse patient outcomes and that reducing NLRP3 slowed cancer cell growth and migration.
- The study highlights NLRP3 as a key player in CRC progression via the epithelial-mesenchymal transition and S6K1-GLI1 pathways, suggesting it could be a valuable target for future cancer therapies.
Article Abstract
Colorectal cancer (CRC) is the primary cause of cancer-related mortality globally. Research indicates that CRC is associated with the dysregulation of NLRP3 expression. Therefore, further investigation is warranted into the correlation between NLRP3 and CRC proliferation and metastasis. NLRP3 and GLI1 expression levels were assessed in tumor tissues using qPCR and bioinformatics analysis. We performed Western blot, CCK8 assay, Colony formation assay, Transwell assay, and mouse xenografts to investigate the effects of NLRP3 on the proliferation and migration of CRC cells while identifying the potential underlying mechanisms involved. Our research demonstrated that elevated NLRP3 levels in CRC tissue correlated with adverse patient outcomes. Enhanced NLRP3 expression significantly affects progression-free and relapse-free survival. Furthermore, suppressing NLRP3 expression effectively inhibited the proliferation and migration of CRC cells while impeding epithelial-mesenchymal transition (EMT) signaling and the S6K1-GLI1 pathway. Notably, the mouse xenotransplantation study validated that deleting NLRP3 suppresses CRC development. NLRP3 facilitates CRC progression via the EMT and the S6K1-GLI1 signaling pathway, providing a promising target against CRC patients.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11685681 | PMC |
| http://dx.doi.org/10.7150/jca.101285 | DOI Listing |
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