ArticleScientific reports2025
PCYT2 mediates ovarian epithelial cancer metastasis by regulating cell membrane fluidity through the AMPK/FOXO1 signalling pathway.
Article in Scientific reports, 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
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
2 citing papers in PubMed.
- PCYT2 inhibits lipid accumulation via the notch signaling pathway in chicken primary hepatocytes.Poultry science · 2026Article
- Evaluating the prognostic value of cuproptosis-related genes and characterizing PDE3B's role in gastric cancer: integrative bioinformatics analysis and experimental validation.Journal of gastrointestinal oncology · 2026Article
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
This study investigates the role of phosphatidylethanolamine cytidylyltransferase 2 (PCYT2) in ovarian epithelial cancer, specifically examining its effects on cell migration and membrane fluidity. To achieve this, we will examine how the AMPK and FOXO1 pathways regulate these processes. Our analysis revealed a significant upregulation of PCYT2 expression in metastatic ovarian cancer tissues compared to primary cancer sites, which correlates with altered membrane fluidity. Our data indicate that PCYT2 is essential for modulating the invasive characteristics of ovarian cancer cells. It does this by regulating the expression levels of AMPK and FOXO1, suggesting its role as an upstream regulator in this signaling pathway. Experiments that either inhibit or enhance PCYT2 activity suggest that it may influence cancer cell infiltration by changing membrane fluidity. These findings provide valuable insights into the molecular mechanisms of ovarian cancer metastasis and highlight PCYT2 as a promising therapeutic target. Future research should validate these findings in larger cohort studies, and also explore the therapeutic potential of targeting PCYT2 in ovarian cancer treatment. In conclusion, although there have been substantial advancements in ovarian cancer therapies, the intricate nature of its metastatic behavior remains a major challenge. Our research clearly demonstrates the critical role of PCYT2, urging the scientific community to deepen their understanding of its involvement in cancer progression and to develop innovative treatment strategies.
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.