ArticleSignal transduction and targeted therapy
Chemical compound cinobufotalin potently induces FOXO1-stimulated cisplatin sensitivity by antagonizing its binding partner MYH9.
Article in Signal transduction and targeted therapy. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
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Who cites it
54 citing papers in PubMed, 84 citations in OpenAlex.
- TET1-mediated DNA demethylation and transcription activation of MRPS17 induces lung adenocarcinoma through PI3K-AKT-mTOR pathway.Journal of molecular histology · 2026Article
- MYH9: Structure, functions, and therapeutic implications in cancer and genetic disorders.Genes & diseases · 2026Review
- Overexpression of FOXO1 may suppress proliferation and migration and correlate with tumor immune cells in nasopharyngeal carcinoma.Translational cancer research · 2026Article
- YTHDF2 enhances proliferation and metastasis of nasopharyngeal carcinoma by mediating m6A modification in destabilizing FOXO1 mRNA.Cancer biology & therapy · 2025Article
- Effect of miR-6767-5p on breast cancer cell phenotype and its regulatory mechanism.Scientific reports · 2025Article
- MYH9 promotes malignant progression of glioma cells through regulating β-catenin stability via epithelial-mesenchymal transition signaling pathway.Scientific reports · 2025Article
- Combined application of BNLF2b antibody with VCA-IgA, Rta-IgG, and Zta-IgA in nasopharyngeal carcinoma screening in the Guangxi region.PloS one · 2025Article
- IncreasedThe Journal of international medical research · 2024Article
- Non-Muscle Myosin II A: Friend or Foe in Cancer?International journal of molecular sciences · 2024Review
- Unveiling the enigmatic role of MYH9 in tumor biology: a comprehensive review.Cell communication and signaling : CCS · 2024Review
- Sesamolin serves as an MYH14 inhibitor to sensitize endometrial cancer to chemotherapy and endocrine therapy via suppressing MYH9/GSK3β/β-catenin signaling.Cellular & molecular biology letters · 2024Article
- Cinobufotalin regulates the USP36/c-Myc axis to suppress malignant phenotypes of colon cancer cellsAging · 2024Article
- Exploring the nexus between MYH9 and tumors: novel insights and new therapeutic opportunities.Frontiers in cell and developmental biology · 2024Review
- Homeobox B2 promotes malignant behavior and contributes to the radioresistance of nasopharyngeal carcinoma by regulating forkhead box protein O1.International journal of medical sciences · 2024Article
- E3 ubiquitin ligases in nasopharyngeal carcinoma and implications for therapies.Journal of molecular medicine (Berlin, Germany) · 2023Article
- Precision medicine in nasopharyngeal carcinoma: comprehensive review of past, present, and future prospect.Journal of translational medicine · 2023Review
- Molecular mechanism underlying epithelial-mesenchymal transformation and cisplatin resistance in esophageal squamous cell carcinoma.Thoracic cancer · 2023Review
- LITAF inhibits colorectal cancer stemness and metastatic behavior by regulating FOXO1-mediated SIRT1 expression.Clinical & experimental metastasis · 2023Article
- MYH10 Combines with MYH9 to Recruit USP45 by Deubiquitinating Snail and Promotes Serous Ovarian Cancer Carcinogenesis, Progression, and Cisplatin Resistance.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- [High expression of MYH9 inhibits apoptosis of non-small cell lung cancer cells through activating the AKT/c-Myc pathway].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2023Article
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Authors and funding
17 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In this study, we present novel molecular mechanisms by which FOXO1 functions as a tumor suppressor to prevent the pathogenesis of nasopharyngeal carcinoma (NPC). First, we observed that FOXO1 not only controlled tumor stemness and metastasis, but also sensitized NPC cells to cisplatin (DDP) in vitro and in vivo. Mechanistic studies demonstrated that FOXO1-induced miR-200b expression through the GSK3β/β-catenin/TCF4 network-mediated stimulation of ZEB1, which reduced tumor stemness and the epithelial-mesenchymal transition (EMT) signal. Furthermore, we observed FOXO1 interaction with MYH9 and suppression of MYH9 expression by modulating the PI3K/AKT/c-Myc/P53/miR-133a-3p pathway. Decreased MYH9 expression not only reduced its interactions with GSK3β, but also attenuated TRAF6 expression, which then decreased the ubiquitin-mediated degradation of GSK3β protein. Increased GSK3β expression stimulated the β-catenin/TCF4/ZEB1/miR-200b network, which increased the downstream tumor stemness and EMT signals. Subsequently, we observed that chemically synthesized cinobufotalin (CB) strongly increased FOXO1-induced DDP chemosensitivity by reducing MYH9 expression, and the reduction in MYH9 modulated GSK3β/β-catenin and its downstream tumor stemness and EMT signal in NPC. In clinical samples, the combination of low FOXO1 expression and high MYH9 expression indicated the worst overall survival rates. Our studies demonstrated that CB potently induced FOXO1-mediated DDP sensitivity by antagonizing its binding partner MYH9 to modulate tumor stemness in NPC.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.