ArticleNature communications2015
The cell cycle regulator 14-3-3σ opposes and reverses cancer metabolic reprogramming.
Article in Nature communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
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Who cites it
57 citing papers in PubMed.
- Covalent Stabilizers of the Interaction Between 14-3-3σ and Estrogen Receptor‑α.ACS medicinal chemistry letters · 2026Article
- Fat promotes growth and invasion in a 3D microfluidic tumor model of triple-negative breast cancer.APL bioengineering · 2026Article
- Riboflavin-PLGA nanoparticles enhance the effectiveness of the pyruvate carboxylase inhibitor ZY-444 in targeting lipogenesis in colon and breast cancer.Scientific reports · 2025Article
- Molecular mechanisms of the Xiao-chai-hu-tang on chronic stress-induced colorectal cancer growth based on an integrated network pharmacology and RNA sequencing approach with experimental validation.BMC complementary medicine and therapies · 2025Article
- Modulation of Protein-Protein Interactions with Molecular Glues in a Synthetic Condensate Platform.Journal of the American Chemical Society · 2025Article
- Article
- Versatility of 14-3-3 proteins and their roles in bone and joint-related diseases.Bone research · 2024Review
- Structural Characterization of Heat Shock Protein 90β and Molecular Interactions with Geldanamycin and Ritonavir: A Computational Study.International journal of molecular sciences · 2024Article
- 14-3-3 Protein-Protein Interactions: From Mechanistic Understanding to Their Small-Molecule Stabilization.Chembiochem : a European journal of chemical biology · 2024Review
- Tumour-specific phosphorylation of serine 419 drives alpha-enolase (ENO1) nuclear export in triple negative breast cancer progression.Cell & bioscience · 2024Article
- Usnic Acid Targets 14-3-3 Proteins and Suppresses Cancer Progression by Blocking Substrate Interaction.JACS Au · 2024Article
- eIF3f Mediates SGOC Pathway Reprogramming by Enhancing Deubiquitinating Activity in Colorectal Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Protein-protein interactions: developing small-molecule inhibitors/stabilizers through covalent strategies.Trends in pharmacological sciences · 2023Review
- Roles of lncRNA LVBU in regulating urea cycle/polyamine synthesis axis to promote colorectal carcinoma progression.Oncogene · 2022Article
- ZLM-7 Blocks Breast Cancer Progression by Inhibiting MDM2 via Upregulation of 14-3-3 Sigma.Pharmaceuticals (Basel, Switzerland) · 2022Article
- Quantitative Proteome Analysis RevealsMolecules (Basel, Switzerland) · 2022Article
- P63 and P73 Activation in Cancers with p53 Mutation.Biomedicines · 2022Review
- 14-3-3ζ Constrains insulin secretion by regulating mitochondrial function in pancreatic β cells.JCI insight · 2022Article
- Filamin-A expression in laryngeal squamous cell carcinoma and its clinical significance.Histology and histopathology · 2022Article
- A Novel Role for RNF126 in the Promotion of G2 Arrest via Interaction With 14-3-3σ.International journal of radiation oncology, biology, physics · 2022Article
Corrections and comments
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Authors and funding
48 authors.
Funding
Abstract
Extensive reprogramming of cellular energy metabolism is a hallmark of cancer. Despite its importance, the molecular mechanism controlling this tumour metabolic shift remains not fully understood. Here we show that 14-3-3σ regulates cancer metabolic reprogramming and protects cells from tumorigenic transformation. 14-3-3σ opposes tumour-promoting metabolic programmes by enhancing c-Myc poly-ubiquitination and subsequent degradation. 14-3-3σ demonstrates the suppressive impact on cancer glycolysis, glutaminolysis, mitochondrial biogenesis and other major metabolic processes of tumours. Importantly, 14-3-3σ expression levels predict overall and recurrence-free survival rates, tumour glucose uptake and metabolic gene expression in breast cancer patients. Thus, these results highlight that 14-3-3σ is an important regulator of tumour metabolism, and loss of 14-3-3σ expression is critical for cancer metabolic reprogramming. We anticipate that pharmacologically elevating the function of 14-3-3σ in tumours could be a promising direction for targeted anticancer metabolism therapy development in future.
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