ArticleFEBS open bio2026
FGFR Like1 drives esophageal cancer progression via EMT, PI3K/Akt, and notch signalling: insights from clinical data and next-generation sequencing analysis.
Article in FEBS open bio, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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.
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Who cites it
1 citing paper in PubMed.
- Elucidating the dual regulation of apoptosis and migration by Ajugasterone C in AGS cells via the PI3K/AKT pathway.Frontiers in pharmacology · 2026Article
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Authors and funding
4 authors.
Funding
Abstract
FGFRL1, one of the least explored FGFRs, has recently been shown to have implications in cancer, but its functional significance in esophageal cancer (EC) remains largely unexplored. We evaluated FGFRL1 expression in EC patients (n = 106) using immunohistochemistry, observing a significant increase in preneoplastic and neoplastic tissues (P < 0.001, OR = 73.2; AUC = 0.817). RNAi-coupled next-generation sequencing revealed enrichment of EMT, PI3K/Akt, and Notch pathways. Quantitative RT-PCR validated the downregulation of top cluster and Notch pathway genes (P < 0.05). Western blot showed decreased phospho-GSK3β, phospho-Akt, and mesenchymal markers. TCGA data supported a positive correlation with EMT. Functional assays demonstrated FGFRL1's oncogenic role, showing G1 phase arrest, and reduced proliferation, migration, and invasion (P < 0.001). Our study highlights FGFRL1 as a key driver of EC progression.
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