AI Article Synopsis
- Uterine corpus endometrial carcinoma (UCEC) is a rapidly increasing cancer type in women, with the Wnt/β-catenin signaling pathway playing a key role in its development.
- FBXO17, a member of the F-box family, is found to be significantly downregulated in UCEC tissues, linked to higher tumor grades and increased cell proliferation in the Ishikawa cell line.
- The study suggests that FBXO17 may act as a novel inhibitor of endometrial tumor growth by regulating the Wnt signaling pathway and influencing the expression of adhesion molecules like E-cadherin and N-cadherin.
Article Abstract
Uterine corpus endometrial carcinoma (UCEC) is one of the most common types of cancer in women, and the incidence is rapidly increasing. Studies have shown that various signaling pathways serve crucial roles in the tumorigenesis of UCEC, amongst which the Wnt/β-catenin pathway is of great interest due to its crucial role in cell proliferation and the huge potential as a therapeutic target. In the present study, it was shown that FBXO17, which is a member of the F-box family, is abnormally downregulated in UCEC tissues compared with non-tumor endometrial tissues, and this was significantly associated with the clinical histological grade, as well as the abnormal proliferation of the UCEC cell line, Ishikawa, both and . Besides, the results suggested that FBXO17 may inhibit the Wnt/β-catenin signaling pathway and influence the expression of adhesion molecules, such as E-cadherin and N-cadherin in Ishikawa cells. In conclusion, these findings indicate that FBXO17 is a novel inhibitor of endometrial tumor development and it likely exerts effects via regulation of the Wnt signaling pathway.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9413558 | PMC |
| http://dx.doi.org/10.7150/ijms.60335 | DOI Listing |
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