ArticleBioscience reports2020
STYX/FBXW7 axis participates in the development of endometrial cancer cell via Notch-mTOR signaling pathway.
Article in Bioscience reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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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
10 citing papers in PubMed, 13 citations in OpenAlex.
- STYX Interacts with FBXW7 to Promote AML Proliferation via Inhibiting the Ubiquitination of CCNE1.Cell biochemistry and biophysics · 2025Article
- Canonical and noncanonical NOTCH signaling in the nongenetic resistance of cancer: distinct and concerted control.Frontiers of medicine · 2025Review
- The Role of FBXW7 in Gynecologic Malignancies.Cells · 2023Review
- Fluorescence in situ hybridization test for detection of endometrial carcinoma cells by non-invasive vaginal swab.Journal of cellular and molecular medicine · 2023Article
- Pseudophosphatase STYX is induced by Helicobacter pylori and promotes gastric cancer progression by inhibiting FBXO31 function.Cell death & disease · 2022Article
- FBXW7 and the Hallmarks of Cancer: Underlying Mechanisms and Prospective Strategies.Frontiers in oncology · 2022Review
- The progress of research into pseudophosphatases.Frontiers in public health · 2022Review
- Pseudophosphatases as Regulators of MAPK Signaling.International journal of molecular sciences · 2021Review
- The FBXW7-NOTCH interactome: A ubiquitin proteasomal system-induced crosstalk modulating oncogenic transformation in human tissues.Cancer reports (Hoboken, N.J.) · 2021Review
- The Roles of Pseudophosphatases in Disease.International journal of molecular sciences · 2021Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Endometrial cancer (EC) is the most common gynecologic malignancy in world. It has been reported that the mutation rate of FBXW7 is frequent in EC, but the specific functions of FBXW7 remain unknown in EC. In the present study, we revealed the role and mechanism of FBXW7 in EC cells. Compared with adjacent nontumor tissues, the FBXW7 expression level was lower in EC tissues. However, the level of STYX was in contrast with the expression of FBXW7 in EC tissues. And STYX interacted with FBXW7 and then down-regulated its expression level in EC. Over-expression of FBXW7 inhibited cell proliferation and facilitated apoptosis in EC cells, whereas silencing FBXW7 acted an opposite effect on EC cells. And the process of FBXW7 participated the proliferation and apoptosis in EC was regulated by STYX. FBXW7 suppressed the expression of Notch pathway related protein, and further inhibited the phosphorylation of mTOR. In addition, we also found that mTOR activitor (MHY1485) and Notch activator (Jagged-1) reversed the effect of over-expressing FBXW7 on cell proliferation and cell apoptosis. And Notch inhibitor (DAPT) counteracted the impact of over-expressing STYX on cell proliferation and cell apoptosis. Collectively, the present study verified that STYX inhibited the expression level of FBXW7 in EC, and then promoted cell proliferation but suppressed apoptosis through Notch-mTOR signaling pathway, which promoted carcinogenesis and progression of EC.
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Registered trials
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