ArticleOncogene2020
SDCBP/MDA-9/syntenin phosphorylation by AURKA promotes esophageal squamous cell carcinoma progression through the EGFR-PI3K-Akt signaling pathway.
Article in Oncogene, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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The trial behind it
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Who cites it
32 citing papers in PubMed, 41 citations in OpenAlex.
- SDCBP Cooperates With YBX1 to Promote ESCC Metastasis by Forming a Positive Feedback Loop With Wnt-β-Catenin Signaling Pathway.Journal of biochemical and molecular toxicology · 2026Article
- Glioblastoma Cells Expressing Oncogenic EGFR Release Multiple Extracellular Vesicle Subpopulations Positive or Negative for EGFR.Journal of extracellular biology · 2026Article
- Decoding SDCBP's role in tumor progression and immune cells infiltration: from databases to macrophage validation.Discover oncology · 2025Article
- Bioinformatics Identification and Experimental Validation of Ferroptosis- and Immune Infiltration-Associated Biomarkers in Ischemic Stroke.Current issues in molecular biology · 2025Article
- Identification of multicohort-based predictive signature for NMIBC recurrence reveals SDCBP as a novel oncogene in bladder cancer.Annals of medicine · 2025Article
- Pre-rRNAs control mitosis by maintaining chromosomal segregation through protecting SMC2 from AURKA-mediated phosphorylation.Cell death & disease · 2025Article
- LincNEAT1 Encoded-NEAT1-31 Promotes Phagocytosis by Directly Activating the Aurora-A-PI3K-AKT Pathway.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Phosphorylation of syntenin-1 by TBK1 promotes proliferation and migration of non-small cell lung cancer cells.The Journal of biological chemistry · 2025Article
- ZNF468/AURKA/PI3K/AKT Positive Feedback Loop Promotes Proliferation and Metastasis of Oesophageal Squamous Cell Carcinoma.Journal of cellular and molecular medicine · 2025Article
- AURKA promotes angiogenesis in uveal melanoma via activation of the JAK2/STAT3/VEGFA signaling pathway.Cancer cell international · 2025Article
- MDA-9/Syntenin as a therapeutic cancer metastasis target: current molecular and preclinical understanding.Expert opinion on therapeutic targets · 2025Review
- The AURKA inhibitor alters the immune microenvironment and enhances targeting B7-H3 immunotherapy in glioblastoma.JCI insight · 2025Article
- Integrated bioinformatics analysis to explore potential therapeutic targets and drugs for small cell carcinoma of the esophagus.Frontiers in bioinformatics · 2025Article
- The significant others of aurora kinase a in cancer: combination is the key.Biomarker research · 2024Review
- Clinical analysis of 10 cases with subcutaneous panniculitis-like T-cell lymphoma and tissue AURKA expression.Skin research and technology : official journal of International Society for Bioengineering and the Skin (ISBS) [and] International Society for Digital Imaging of Skin (ISDIS) [and] International Society for Skin Imaging (ISSI) · 2024Article
- Dexrazoxane inhibits the growth of esophageal squamous cell carcinoma by attenuating SDCBP/MDA-9/syntenin-mediated EGFR-PI3K-Akt pathway activation.Scientific reports · 2024Article
- Recent Updates on Oncogenic Signaling of Aurora Kinases in Chemosensitive, Chemoresistant Cancers: Novel Medicinal Chemistry Approaches for Targeting Aurora Kinases.Current medicinal chemistry · 2024Review
- NUMA1 modulates apoptosis of esophageal squamous cell carcinoma cells through regulating ASK1-JNK signaling pathway.Cellular and molecular life sciences : CMLS · 2023Article
- Lysine butyrylation of HSP90 regulated by KAT8 and HDAC11 confers chemoresistance.Cell discovery · 2023Article
- E2F1-mediated KDM4A-AS1 up-regulation promotes EMT of hepatocellular carcinoma cells by recruiting ILF3 to stabilize AURKA mRNA.Cancer gene therapy · 2023Article
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
SDCBP is an adapter protein containing two tandem PDZ domains mediating cell adhesion. The role and underlying molecular mechanism of SDCBP in ESCC remain obscure. Here, we report that SDCBP is frequently overexpressed in ESCC tissues and cells compared to normal controls and that its overexpression is correlated with late clinical stage and predicts poor prognosis in ESCC patients. Functionally, high expression of SDCBP is positively related to ESCC progression both in vitro and in vivo. Furthermore, mechanistic studies show that SDCBP activates the EGFR-PI3K-Akt signaling pathway by binding to EGFR and preventing EGFR internalization. Moreover, we provide evidence that AURKA binds to SDCBP and phosphorylates it at the Ser131 and Thr200 sites to inhibit ubiquitination-mediated SDCBP degradation. More importantly, the sites at which AURKA phosphorylates SDCBP are crucial for the EGFR signaling-mediated oncogenic function of SDCBP. Taken together, we propose that SDCBP phosphorylation by AURKA prevents SDCBP degradation and promotes ESCC tumor growth through the EGFR-PI3K-Akt signaling pathway. Our findings unveil a new AURKA-SDCBP-EGFR axis that is involved in ESCC progression and provide a promising therapeutic target for ESCC treatment in the clinic.
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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.