ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2023
SAMD9 Promotes Postoperative Recurrence of Esophageal Squamous Cell Carcinoma by Stimulating MYH9-Mediated GSK3β/β-Catenin Signaling.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 33 citations in OpenAlex.
- Regulatory mechanism of the RNF168-SCCA1-MYH9 signaling axis in the response of ulcerative colitis.Journal of gastroenterology · 2026Article
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- FAM107A inhibits Invasion and migration of colorectal cancer by affecting EMT via the AKT pathway.Histology and histopathology · 2026Article
- VCAN promotes the progression and recurrence of esophageal squamous cell carcinoma by remodeling the tumor microenvironment.Scientific reports · 2026Article
- Gastric and upper gastrointestinal oncology: integrating breakthroughs from prevention to precision therapeutics.Experimental hematology & oncology · 2026Article
- Enhanced oral nanomedicine utilizing biomineralized oncolytic virus for synergistic gastrointestinal cancer therapy.Materials today. Bio · 2025Article
- Chimeric antigen receptor modified hematopoietic stem cells (CAR-HSCs) arm all immune forces for anti-tumor in mice.Experimental hematology & oncology · 2025Article
- SLIT2 modulates NMIIA to regulate mitophagy and suppress hepatocellular carcinoma progression.BMC cancer · 2025Article
- The immune microenvironment of pathogen-associated cancers and current clinical therapeutics.Molecular cancer · 2025Review
- ARHGAP4/MYH9/β-catenin/c-Jun positive feedback loop promotes colorectal cancer stemness.NPJ precision oncology · 2025Article
- ACSS2 coupled with KAT7 regulates histone β-hydroxybutyrylation to enhance transcription.Science advances · 2025Article
- Decoding the metabolic dialogue in the tumor microenvironment: from immune suppression to precision cancer therapies.Experimental hematology & oncology · 2025Review
- Role of myosin heavy chain 9 in gastrointestinal tumorigenesis: A comprehensive review.World journal of gastrointestinal oncology · 2025Review
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- New insights into the role of ubiquitination in angiogenesis (Review).International journal of molecular medicine · 2025Review
- M2-like Macrophages-derived CCL17 Promotes Esophageal Squamous Cell Carcinoma Metastasis and Stemness via Activating CCR4-mediated ERK/PD-L1 Pathway.Current molecular medicine · 2025Article
- Epigenetic silencingCancer biology & therapy · 2024Article
- Targeting the SPC25/RIOK1/MYH9 Axis to Overcome Tumor Stemness and Platinum Resistance in Epithelial Ovarian Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Wnt signaling aberrant activation drives ameloblastoma invasion and recurrence: bioinformatics and in vitro insights.BMC oral health · 2024Article
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 1 country.
Funding
Abstract
Recurrence is a challenge to survival after the initial treatment of esophageal squamous cell carcinoma (ESCC). But, its mechanism remains elusive and there are currently no biomarkers to predict postoperative recurrence. Here, the possibility of sterile alpha motif domain-containing protein 9 (SAMD9) as a predictor of postoperative recurrence of ESCC is evaluated and the molecular mechanisms by which SAMD9 promotes ESCC recurrence are elucidated. The authors found that the high level of SAMD9 is correlated with postoperative recurrence and poor prognosis of ESCC. Overexpression of SAMD9 promotes tumor stemness, angiogenesis, and EMT, while downregulation of SAMD9 reduced these phenotypes. Mechanistically, it is found that SAMD9 stimulated ubiquitination-mediated glycogen synthase kinase-3 beta (GSK-3β) degradation by interaction with myosin-9 (MYH9) and TNF receptor-associated factor 6 (TRAF6), which in turn activated Wnt/β-catenin pathway. Further, the authors demonstrated that silencing SAMD9 inhibited lung metastasis and tumor formation in vivo. Finally, the authors found that silencing MYH9 or β-catenin, or overexpressing GSK-3β inhibited SAMD9-stimulated ESCC cell stemness, EMT, angiogenesis, metastasis, and tumorigenicity. Together, the findings indicate that the SAMD9/MYH9/GSK3β/β-catenin axis promotes ESCC postoperative recurrence and that SAMD9 is a crucial target for ESCC therapy. Additionally, SAMD9 has the potential as a predictor of postoperative recurrence in ESCC.
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Registered trials
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.