ArticleJournal of ovarian research2026
IL-24 amplifies baicalein-induced immunogenic cell death in ovarian cancer by boosting endoplasmic reticulum stress.
Article in Journal of ovarian research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
Abstract
backgroundOvarian cancer (OC) remains a leading cause of gynecologic cancer mortality worldwide, highlighting the need for novel immunomodulatory therapies. Immunogenic cell death (ICD) has emerged as a promising strategy to enhance antitumor immunity in OC. Baicalein, a bioactive flavonoid with documented anticancer activity across diverse tumor types, has not been comprehensively assessed for its potential to induce ICD in OC. This study aimed to explore baicalein’s ability to promote ICD and elucidate the underlying molecular mechanisms.
methodsBoth murine (ID8) and human (SKOV3) ovarian cancer cell lines were used to examine the cytotoxic and immunogenic effects of baicalein. Cell viability and apoptosis were evaluated using CCK-8 assays and flow cytometry. ICD hallmarks, including surface calreticulin (CRT) exposure, extracellular ATP and HMGB1 release, as well as the induction of pro-inflammatory cytokines, were systematically evaluated in cells treated with baicalein. The functional impact on immune activation was assessed in vitro using dendritic cells and in vivo via T cell priming assays. RNA-sequencing and RT-PCR were used to explore underlying molecular pathways, including endoplasmic reticulum (ER) stress signaling and IL-24 induction.
resultsWe found that OC cells treated with baicalein showed increased ICD features, including CRT exposure, extracellular release of ATP and HMGB1, and increased expression of IFNβ and CXCL10. Functionally, baicalein-treated OC cells promoted dendritic cell maturation and stimulated CD4⁺ and CD8⁺ T cell responses in vivo. Transcriptomic analysis revealed activation of ER stress pathways, particularly the ATF3/CHOP/DR5 axis. Inhibition of ER stress or reactive oxygen species (ROS) attenuated baicalein-induced ICD, suggesting a ROS-dependent mechanism. Notably, baicalein markedly upregulated IL-24 expression in an ER stress-dependent manner and IL-24 further enhanced baicalein-induced ER stress and ICD features.
conclusionThis study reveals that BAI induces IL-24 expression through ER stress, with IL-24 subsequently reinforcing BAI-mediated ER stress and potentiating ICD in ovarian cancer. These findings support the therapeutic potential of BAI as an ICD inducer and immunomodulatory agent in ovarian cancer.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.