ArticleCell death & disease2014
Inhibitory effect of 2-(piperidinoethoxyphenyl)-3-(4-hydroxyphenyl)-2H-benzo(b)pyran (K-1) on human primary endometrial hyperplasial cells mediated via combined suppression of Wnt/β-catenin signaling and PI3K/Akt survival pathway.
Article in Cell death & disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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14 citing papers in PubMed, 29 citations in OpenAlex.
- Identification and Validation of a Four-Gene Signature as a Novel Potential Diagnostic Biomarker Panel for Endometriosis: Causal and Mechanistic Insights from Mendelian Randomization and Bioinformatics.International journal of women's health · 2026Article
- From Inflammation to Malignancy: The Link Between Endometriosis and Gynecological Cancers.International journal of molecular sciences · 2025Review
- Effect of 2-methoxyestradiol on mammary tumor initiation and progression.Cancer reports (Hoboken, N.J.) · 2024Article
- Senegenin Inhibits AβNeuropsychiatric disease and treatment · 2022Article
- FBXO17 Inhibits the Wnt/β-Catenin Pathway and Proliferation of Ishikawa Cells.International journal of medical sciences · 2022Article
- Targeting Wnt Signaling in Endometrial Cancer.Cancers · 2021Review
- miR‑593 inhibits proliferation and invasion and promotes apoptosis in non‑small cell lung cancer cells by targeting SLUG‑associated signaling pathways.Molecular medicine reports · 2019Article
- Inflammatory-Related P62 Triggers Malignant Transformation of Mesenchymal Stem Cells through the Cascade of CUDR-CTCF-IGFII-RAS Signaling.Molecular therapy. Nucleic acids · 2018Article
- miR372 Promotes Progression of Liver Cancer Cells by Upregulating erbB-2 through Enhancement of YB-1.Molecular therapy. Nucleic acids · 2018Article
- Long noncoding RNA MEG3 suppresses liver cancer cells growth through inhibiting β-catenin by activating PKM2 and inactivating PTEN.Cell death & disease · 2018Article
- Inhibition of WNT7A-β-catenin signaling pathway sensitizes oral squamous cell carcinoma to cisplatin.International journal of clinical and experimental pathology · 2018Article
- FOXP1 forkhead transcription factor is associated with the pathogenesis of endometrial cancer.Heliyon · 2016Article
- Therapeutic options for management of endometrial hyperplasia.Journal of gynecologic oncology · 2016Review
- Inhibition of the Tcf/beta-catenin complex increases apoptosis and impairs adrenocortical tumor cell proliferation and adrenal steroidogenesis.Oncotarget · 2015Article
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9 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Endometrial hyperplasia is a precursor to the most common gynecologic cancer diagnosed in women. Apart from estrogenic induction, aberrant activation of the Wnt/β-catenin signal is well known to correlate with endometrial hyperplasia and its carcinoma. The benzopyran compound 2-(piperidinoethoxyphenyl)-3-(4-hydroxyphenyl)-2H-benzo (b) pyran(K-1), a potent antiestrogenic agent, has been shown to have apoptosis-inducing activity in rat uterine hyperplasia. The current study was undertaken to explore the effect of the benzopyran compound K-1 on growth and Wnt signaling in human endometrial hyperplasial cells. Primary culture of atypical endometrial hyperplasial cells was characterized by the epithelial cell marker cytokeratin-7. Results revealed that compound K-1 reduced the viability of primary endometrial hyperplasial cells and expression of ERα, PR, PCNA, Wnt7a, FZD6, pGsk3β and β-catenin without affecting the growth of the primary culture of normal endometrial cells. The β-catenin target genes CyclinD1 and c-myc were also found to be reduced, whereas the expression of axin2 and Wnt/β-catenin signaling inhibitor Dkk-1 was found to be upregulated, which caused the reduced interaction of Wnt7a and FZD6. Nuclear accumulation of β-catenin was found to be decreased by compound K-1. K-1 also suppressed the pPI3K/pAkt survival pathway and induced the cleavage of caspases and PARP, thus subsequently causing the apoptosis of endometrial hyperplasial cells. In conclusion, compound K-1 suppressed the growth of human primary endometrial hyperplasial cells through discontinued Wnt/β-catenin signaling and induced apoptosis via inhibiting the PI3K/Akt survival pathway.
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