ArticleMolecular biology reports2025
Phospholipase Cε1 activates Rap1 signaling pathway to promote proliferation, EMT and angiogenesis of choriocarcinoma cells.
Article in Molecular biology 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.
- Unravelling Multilayered RNA Modification Networks in Female Reproduction and Obstetric/Gynaecologic Disorders.Biomolecules · 2026Review
- Structural insights into Phospholipase Cε activity and regulation.The Journal of biological chemistry · 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
5 authors.
Funding
Abstract
backgroundChoriocarcinoma is a rare yet highly malignant gestational trophoblastic tumor, and its molecular mechanisms remain largely unclear. This study reveals the critical role of phospholipase Cε1 (PLCE1) in the malignant progression of choriocarcinoma and its epigenetic regulatory mechanisms.
methodsThe GSE88873 dataset was analyzed to assess PLCE1 expression in choriocarcinoma. PLCE1 expression was then quantified in choriocarcinoma tissues and cell lines (JAR and BEWO) versus normal trophoblastic controls using RT-qPCR and Western blot analysis. Functional verification assays were performed via PLCE1 knockdown in choriocarcinoma cell lines.
resultsAnalysis of GSE88873 demonstrated significant overexpression of PLCE1 in choriocarcinoma cell lines, with pan-cancer analysis showing its widespread upregulation in various tumors. Both mRNA and protein expression levels of PLCE1 were markedly elevated in choriocarcinoma tissues and cell lines compared to normal trophoblastic tissues and cells. PLCE1 knockdown suppressed choriocarcinoma cell proliferation, induced apoptosis, and reversed epithelial-mesenchymal transition (EMT). Notably, PLCE1 silencing significantly impaired the tube-forming capacity of vascular endothelial cells induced by choriocarcinoma-conditioned medium. Mechanistic investigations further demonstrated that PLCE1 mRNA contains abundant m6A modification sites, with methyltransferase METTL14 enhancing its stability through m6A modification. Additionally, PLCE1 activates the Rap1 signaling pathway to promote downstream VEGF secretion, and Rap1 activation reverses the PLCE1 knockdown-induced suppression of cell proliferation, EMT blockade, and diminished angiogenic capacity.
conclusionsIn summary, this study is the first to elucidate that PLCE1 maintains high expression via METTL14-mediated m6A methylation, subsequently driving choriocarcinoma cell proliferation, EMT, and angiogenesis through activation of the Rap1/VEGF axis.
Indexed as
Identifiers
40760271What 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.