MiR-624-5p enhances NLRP3 augmented gemcitabine resistance via EMT/IL-1β/Wnt/β-catenin signaling pathway in ovarian cancer.

The current study investigates the NLRP3's cytotoxicity inhibitory effect among ovarian cancer cells and how it interacts with Wnt/β-catenin in vitro conditions. Further, the study also analyzed the regulatory role of NLRP3 in resistance to gemcitabine among ovarian cancer cells and its underlying interaction mechanisms with Wnt/β-catenin in vitro. The current in vitro study detailed that when downregulating NLRP3, it could enhance the gemcitabine sensitivity in GRC cells. In case of gemcitabine-resistant cells, the up-regulation of NLRP3 can increase the drug-resistance through the activation of IL-1β, EMT and Wnt/β-catenin signaling pathways. High expression of miR-624-5p was recorded in ovarian drug resistant cancer cells and it also boosted the cell viabilities. NLRP3 can reinstate the functioning of miR-624-5p in drug resistant cells. This phenomenon concludes that NLRP3 is a promising therapeutic target and can be implemented in traditional chemotherapy to increase the efficacy of the treatment. The current study conducted in vitro experiments and the findings infer that the downregulation of NLRP3 can enhance the sensitivity of gemcitabine among GRC cells. This mechanism will increase the treatment efficacy by inhibiting the drug resistance in GRC. These two entities are the new promising biomarkers that can be used in the detection of platinum resistance in ovarian cancer patients and conduct novel clinical research.