ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
Identification of a Novel Substrate for eEF2K and the AURKA-SOX8 as the Related Pathway in TNBC.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. 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.
- Integrative multi-omics identifies a glycosylation-based prognostic framework and nominates ALG3 for targeted therapy in bladder cancer.Discover oncology · 2026Article
- Exosomal circPOLK promotes metastasis of NSCLC cells via regulating mir-1204/SOX8 axis.Cancer cell international · 2026Article
- Targeted Degradation of eEF2K by a Structure-Guided PROTAC Strategy for the Treatment of Triple-Negative Breast Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- SOX8/CPT2 axis regulates lipid metabolism to support enzalutamide resistance in prostate cancer.Cancer cell international · 2026Article
- eEF2K-Mediated Stabilization of PCBP2 Promotes Oncogenic mRNA Programs in Triple-Negative Breast Cancer.International journal of biological sciences · 2026Article
- Autophagy-Related Proteins in Triple-Negative Breast Cancer: From Molecular Insights to Therapeutic Applications.International journal of molecular sciences · 2025Review
- Harnessing artificial intelligence to identify Bufalin as a molecular glue degrader of estrogen receptor alpha.Nature communications · 2025Article
- Identification of a Novel Substrate for eEF2K and the AURKA-SOX8 as the Related Pathway in TNBC.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
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Authors and funding
16 authors.
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Abstract
Eukaryotic elongation factor 2 kinase (eEF2K) has been considered as a putative target for cancer therapy; however, the underlying mechanisms of eEF2K in triple-negative breast cancer (TNBC) progression remain to be fully elucidated. In this study, it is shown that eEF2K is highly expressed in TNBC and is associated with poor prognosis. In vitro, in vivo, and patient-derived organoid experiments demonstrate that knockdown of eEF2K significantly impedes progression of TNBC. Proteomic analysis and confirmation experiments reveal that eEF2K positively regulates the mRNA and protein expressions of sex-determining region Y-box 8 (SOX8). Mechanistically, eEF2K binds to and phosphorylates aurora kinase A (AURKA) at S391, a newly identified phosphorylation site critical for maintaining AURKA protein stability and kinase activity. Moreover, the compound C1, a molecular glue to degrade eEF2K, is optimized by designing and synthesizing its derivatives using reasonable structure-based optimization approach. The new compound C4 shows better ability to degrade eEF2K and stronger anti-cancer activity than C1. These findings not only uncover the pivotal role of the eEF2K/AURKA/SOX8 axis in TNBC progression, but also provide a promising lead compound for developing novel drug for treatment of TNBC.
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