ArticleNature communications2020
Mutant p53 induces Golgi tubulo-vesiculation driving a prometastatic secretome.
Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 1 of them a synthesis that pooled it.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
50 citing papers in PubMed, 1 synthesis or guideline pooled it, 93 citations in OpenAlex.
- Loss of p53-DREAM-mediated repression of cell cycle genes as a driver of lymph node metastasis in head and neck cancer.Genome medicine · 2023Pooled it
- The Dynamic Alliance of p53 and Metabolism in the Tumor Microenvironment Shapes Tumor Evolution.BioEssays : news and reviews in molecular, cellular and developmental biology · 2026Review
- TP53 mutation at codon 179 metabolically reprograms cancer cells to promote invasion.Cancer gene therapy · 2026Article
- Differential AXL expression and Arf1 regulation control stiffness-dependent Golgi organization in breast cancer cells.Journal of cell science · 2026Article
- Common oncogenic mutations in colorectal cancer: drivers of carcinogenesis and potential therapeutic targets.Frontiers in pharmacology · 2026Review
- Predictive effect and clinical diagnosis significance of exosome-related genes for nonalcoholic fatty liver disease-related hepatocellular carcinoma.Scientific reports · 2025Article
- p53: A player in the tumor microenvironment.Oncology research · 2025Review
- Expression and Significance of PI3K p85α and p53 Protein in Colorectal Cancer Tissues.Cancer management and research · 2025Article
- Review
- SNPs Give LACTB Oncogene-Like Functions and Prompt Tumor Progression via Dual-Regulating p53.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Cancer cell stiffening via CoQNature communications · 2024Article
- p53 at the crossroads of tumor immunity.Nature cancer · 2024Review
- Recent Advances on Mutant p53: Unveiling Novel Oncogenic Roles, Degradation Pathways, and Therapeutic Interventions.Biomolecules · 2024Review
- Engineered Adoptive T-Cell Therapies for Breast Cancer: Current Progress, Challenges, and Potential.Cancers · 2023Review
- Mutant p53-ENTPD5 control of the calnexin/calreticulin cycle: a druggable target for inhibiting integrin-α5-driven metastasis.Journal of experimental & clinical cancer research : CR · 2023Article
- The Tumor Suppressor DAB2IP Is Regulated by Cell Contact and Contributes to YAP/TAZ Inhibition in Confluent Cells.Cancers · 2023Article
- Recent Advances in Transcription Factors Biomarkers and Targeted Therapies Focusing on Epithelial-Mesenchymal Transition.Cancers · 2023Review
- Homogenous TP53mut-associated tumor biology across mutation and cancer types revealed by transcriptome analysis.Cell death discovery · 2023Article
- EMT-activated secretory and endocytic vesicular trafficking programs underlie a vulnerability to PI4K2A antagonism in lung cancer.The Journal of clinical investigation · 2023Article
- A combined experimental-computational approach uncovers a role for the Golgi matrix protein Giantin in breast cancer progression.PLoS computational biology · 2023Article
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Authors and funding
24 authors at 11 institutions in 3 countries.
Funding
Abstract
TP53 missense mutations leading to the expression of mutant p53 oncoproteins are frequent driver events during tumorigenesis. p53 mutants promote tumor growth, metastasis and chemoresistance by affecting fundamental cellular pathways and functions. Here, we demonstrate that p53 mutants modify structure and function of the Golgi apparatus, culminating in the increased release of a pro-malignant secretome by tumor cells and primary fibroblasts from patients with Li-Fraumeni cancer predisposition syndrome. Mechanistically, interacting with the hypoxia responsive factor HIF1α, mutant p53 induces the expression of miR-30d, which in turn causes tubulo-vesiculation of the Golgi apparatus, leading to enhanced vesicular trafficking and secretion. The mut-p53/HIF1α/miR-30d axis potentiates the release of soluble factors and the deposition and remodeling of the ECM, affecting mechano-signaling and stromal cells activation within the tumor microenvironment, thereby enhancing tumor growth and metastatic colonization.
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What Socratic holds
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 Socratic graph.