ArticleFrontiers in cell and developmental biology2026
The innate immune mediator group IIA secreted phospholipase A
Article in Frontiers in cell and developmental biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Human Group IIA Secreted Phospholipase AInternational journal of molecular sciences · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: We and others have shown that elevated human Group IIA secreted phospholipase A Methods: We have used established patient-derived androgen-independent prostate cancer (PCa) cell lines, DU145, PC-3 and vimentin-knockout DU145 (DU145 Results: We found that addition of exogenous hGIIA increased LD metabolism as evidenced by LD immunofluorescence signal and this increase is dependent on vimentin in PCa. The response is dependent on hGIIA levels with high concentrations of hGIIA associated with PLIN2 loss, PLIN3 suppression, and DGAT1 induction without FASN upregulation. Kesonotide alone was largely inert. However, at high concentration of hGIIA, Kesonotide attenuated lipid metabolism by neutralizing perilipin remodelling and attenuating DGAT1 induction in knockout cells. Discussion: Taken together, these findings identify a context-dependent hGIIA LD-remodelling program that is shaped by vimentin, implicating for the first time the hGIIA-vimentin axis in inflammatory cue-driven lipid metabolic rewiring in aggressive PCa.
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.