ArticleJournal of ovarian research2025
Inflammasome activation contributes to cisplatin resistance in ovarian cancer.
Article in Journal of ovarian research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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Who cites it
2 citing papers in PubMed.
- Arvanil reverses cisplatin resistance in ovarian cancer by activating HMOX1-driven ferroptosis.Scientific reports · 2026Article
- The NLRP3 inflammasome in gynecological cancers: a double-edged sword shaping the immune microenvironment and immunotherapy response.Frontiers in immunology · 2026Review
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Authors and funding
7 authors.
Funding
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Abstract
backgroundEpithelial ovarian cancer (EOC) is an alarming malignancy with frequent relapse and resistance to chemotherapy. Understanding the mechanism related to these phenotypes is urgent. Here, we investigated the roles of inflammasomes, NLRP1 and NLRP3, and pyroptosis in EOC progression and resistance to treatment.
methodsCell viability under cisplatin (CDDP) treatment was measured with diphenyltetrazolium bromide (MTT), and the IC50 values were calculated for the A2780, ACRP, and OVCAR3 cell lines. The levels of cytokines (interleukin-1β, IL-6, and TNFα) present in the supernatant were measured via ELISA. Caspase-1 activation was detected through the Caspase-Glo® 1 Assay. The cell death profile was determined via flow cytometry using Annexin V/PI staining, and the formation of pores in the cell membrane was measured using PI. A wound healing assay was used to investigate the effects of treatment with CDDP combined with a caspase-1 inhibitor (Ac-YVAD-CHO) on cell migration.
resultsIC50 values indicate increasing CDDP resistance across the following cell lines: A2780 (10.41 μM), ACRP (35.92 μM), and OVCAR3 (43.52 μM). Cytokine secretion and Caspase-1 activation were greater in treated cells than in untreated cells. CDDP-treated cells exhibited increased lytic cell death and pore formation. Caspase-1 inhibition during treatment with CDDP reduced wound closure, indicating reduced cell migration.
conclusionOur findings suggest that inflammasome activation and pyroptosis are mechanisms associated with ovarian cancer chemoresistance to CDDP, contributing to the devastating scenario of this disease. Targeting the NLRP1 and NLRP3 pathways could represent a promising strategy to improve OC treatment.
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