ArticleThe Journal of endocrinology2024
Loss of KLF15 impairs endometrial receptivity by inhibiting EMT in endometriosis.
Article in The Journal of endocrinology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 11 citations in OpenAlex.
- PARP-1 couples β-catenin/TCF4 signaling to epithelial-mesenchymal transition in endometriosis.Scientific reports · 2026Article
- From local lesion to multisystem disease: integrated crosstalk among the gut microbiota, immune system, and host metabolism in endometriosis.Frontiers in immunology · 2026Review
- Clinicopathological significance of Kruppel-like factor 15 and epithelial-to-mesenchymal transition related factors in bladder cancer.Scientific reports · 2025Article
- Machine learning prediction of clinical pregnancy in endometriosis patients following fresh IVF/ICSI-ET.European journal of medical research · 2025Article
- The SOX18-OTUB1-YAP1 axis: a new endometriosis target.Journal of translational medicine · 2025Article
- Krüppel-like factors family in health and disease.MedComm · 2024Review
- Endometrial E-cadherin and N-cadherin Expression during the Mid-Secretory Phase of Women with Ovarian Endometrioma or Uterine Fibroids.Journal of personalized medicine · 2024Article
- [Establishment of a predictive nomogram for clinical pregnancy rate in patients with endometriosis undergoing fresh embryo transfer].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2024Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The impaired endometrial receptivity is a major factor contributing to infertility in patients with endometriosis (EM), but the underlying mechanism remains unclear. Our study aimed to investigate the role of Kruppel-like factor 15 (KLF15) in endometrial receptivity and its regulation in EM. We observed a significant decrease in KLF15 expression in the mid-secretory epithelial endometrial cells of EM patients compared to normal females without EM. To confirm the role of KLF15 in endometrial receptivity, we found a significantly reduced KLF15 expression and a significant decrease in embryo implantation number in the rat model via uterine horn infection with siRNA. This highlights the importance of KLF15 as a regulator receptivity. Furthermore, through ChIP-qPCR, we discovered that the progesterone receptor (PR) directly binds to KLF15 promoter regions, indicating that progesterone resistance may mediate the decrease in KLF15 expression in EM patients. Additionally, we found that the mid-secretory endometrium of EM patients exhibited impaired epithelial-mesenchymal transition (EMT). Knockdown of KLF15 upregulated E-cadherin and downregulated vimentin expression, leading to inhibited invasiveness and migration of Ishikawa cells. Overexpression KLF15 promotes EMT, invasiveness, and migration ability, and increases the attachment rate of JAR cells to Ishikawa cells. Through RNA-seq analysis, we identified TWIST2 as a downstream gene of KLF15. We confirmed that KLF15 directly binds to the promoter region of TWIST2 via ChIP-qPCR, promoting epithelial cell EMT during the establishment of endometrial receptivity. Our study reveals the involvement of KLF15 in the regulation of endometrial receptivity and its downstream effects on EMT. These findings provide valuable insights into potential therapeutic approaches for treating non-receptive endometrium in patients with EM.
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