ArticleExperimental and therapeutic medicine2024
KLF9‑regulated FBXO31 inhibits the progression of endometrial cancer and enhances the sensitivity of endometrial cancer cells to cisplatin.
Article in Experimental and therapeutic medicine, 2024. 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, 2 citations in OpenAlex.
- Survival-Associated Molecular and Epigenetic Alterations in Endocervical Adenocarcinoma: An Exploratory TCGA Multi-Omics Cohort Study.Current issues in molecular biology · 2026Article
- KLF9 in cancer: a potential prognostic marker and therapeutic target.Frontiers in oncology · 2025Review
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Endometrial cancer (EC) is one of the most common malignancies with an increasing annual incidence. F-box only protein 31 (FBXO31) plays a significant regulatory role in several types of cancer. The transcription factor Krüppel-like factor 9 (KLF9) of FBXO31 is reduced in EC as a tumor suppressor. However, their particular regulatory role and mechanism in EC have not been previously reported. Therefore, the UALCAN database was used to predict the expression levels of FBXO31 in EC. In addition, the regulatory effect of FBXO31 on EC cell proliferation, invasion, migration, apoptosis and cisplatin (DDP) sensitivity was investigated at the cellular level. The association between KLF9 and FBXO31 was predicted using the JASPAR database and verified by chromatin immunoprecipitation and luciferase reporter assays. Finally, the regulatory effects of KLF9 and FBXO31 overexpression or silencing were also explored. The results demonstrated that FBXO31 was poorly expressed in EC. Additionally, FBXO31 overexpression inhibited the malignant progression of EC cells and enhanced their sensitivity to DDP. Furthermore, KLF9 promoted FBXO31 transcription. Overall, the present study suggested that the KLF9-mediated regulation of FBXO31 could inhibit the progression of EC and enhance the sensitivity of EC cells to DDP.
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Registered trials
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