ArticleCell and tissue research2021
FGFR4 promotes nuclear localization of GABP to inhibit cell apoptosis in uterine leiomyosarcoma.
Article in Cell and tissue research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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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.
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Who cites it
2 citing papers in PubMed, 6 citations in OpenAlex.
- Therapeutic Vulnerabilities of the Key Genetic Drivers in Leiomyosarcoma.Medical sciences (Basel, Switzerland) · 2026Review
- The immortality mechanism of TERT promoter mutant cancers is self-reinforcing and reversible.Molecular cell · 2025Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
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Abstract
Fibroblast growth factor receptor 4 (FGFR4) has been indicated as a potential "oncogene" in various types of cancer. However, the effects and underlying mechanisms of FGFR4 on uterine leiomyosarcoma (ULMS) progression remain unclear. In this study, we firstly discovered that FGFR4 was upregulated in ULMS specimens and cell lines and closely associated with poor prognosis of ULMS patients. Cell viability and apoptosis assays showed that FGFR4 deletion inhibited cell proliferation and promoted cell apoptosis. Moreover, FGFR4 silence increased cytoplasmic GABP (GA binding protein) expression, while it decreased the nuclear GABP level to inhibit nuclear localization of GABP. Mechanistically, the inhibition ability of FGFR4 silence on nuclear localization of GABP was mediated via mammalian Ste20-like kinases 1 (MST1) activation, which could promote phosphorylation of large tumor suppressor 1 (LATS1) to reduce nuclear localization of GABP. Gain- and loss-of-functional assays indicated that FGFR4 promoted nuclear localization of GABP to inhibit cell apoptosis in ULMS. In conclusion, our findings indicated that FGFR4 inhibited cell apoptosis in ULMS via the promotion of MST1/LATS1-mediated GABP nuclear localization, shedding light on the underlying mechanism of FGFR4-induced ULMS progression.
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