ArticleScience advances2021
p53 loss activates prometastatic secretory vesicle biogenesis in the Golgi.
Article in Science advances, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 33 citations in OpenAlex.
- GPNMB promotes double-membrane vesicle accumulation and facilitates structural protein transport during PEDV infection.Virulence · 2026Article
- PAQR11: An evolutionarily conserved Golgi receptor governing metabolic-immune crosstalk and systemic homeostasis.Histology and histopathology · 2026Review
- EMT activates ER-to-Golgi trafficking through upregulation of REEP2 to promote lung cancer progression.Research square · 2026Article
- Identification of an Anoikis-Related Gene Signature to Predict the Prognosis in Patients With Oral Squamous Cell Carcinoma.International dental journal · 2026Article
- Porcine reproductive and respiratory syndrome virus exploits ESCRT-II subunit EAP20 for entry and replication.Journal of virology · 2026Article
- Osimertinib activates a TGF-β2-dependent secretory program that drives lung adenocarcinoma progression.The Journal of clinical investigation · 2026Article
- Baicalein inhibits the progression of thyroid cancer by suppressing the TPL2/MEK2/ERK2 pathway.Frontiers in endocrinology · 2026Article
- Precise subcellular organelle-targeted analyses of hepatotoxicity ofChinese herbal medicines · 2026Article
- EMT activates ER-to-Golgi trafficking through upregulation of REEP2 to promote lung cancer progression.bioRxiv : the preprint server for biology · 2025Article
- Inference of cell-type composition and single-cell spatial maps from spatial transcriptomics data with SWOT.Communications biology · 2025Article
- Monensin suppresses EMT-driven cancer cell motility by inducing Golgi pH-dependent exocytosis of GOLIM4.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Dichotomous roles of ACBD3 in NSCLC growth and metastasis.Oncogene · 2025Article
- Tailoring Tumor Cell Golgi Apparatus-Targeting Self-Assembled Peptide for Effective Immunotherapy via Reshaping MIF-Mediated Immunosuppressive Network.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Disulfidptosis links the pathophysiology of ulcerative colitis and immune infiltration in colon adenocarcinoma.Scientific reports · 2025Article
- Expression and Significance of PI3K p85α and p53 Protein in Colorectal Cancer Tissues.Cancer management and research · 2025Article
- Review
- Impact of clonal TP53 mutations with loss of heterozygosity on adjuvant chemotherapy and immunotherapy in gastric cancer.British journal of cancer · 2024Article
- The cancer-associated secretory phenotype: a new frontier in targeted therapeutics.The Journal of clinical investigation · 2024Review
- Identification of a Novel Oxidative Stress- and Anoikis-Related Prognostic Signature and Its Immune Landscape Analysis in Non-Small Cell Lung Cancer.International journal of molecular sciences · 2023Article
- MMD collaborates with ACSL4 and MBOAT7 to promote polyunsaturated phosphatidylinositol remodeling and susceptibility to ferroptosis.Cell reports · 2023Article
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
Abstract
Cancer cells exhibit hyperactive secretory states that maintain cancer cell viability and remodel the tumor microenvironment. However, the oncogenic signals that heighten secretion remain unclear. Here, we show that p53 loss activates prometastatic secretory vesicle biogenesis in the Golgi. p53 loss up-regulates the expression of a Golgi scaffolding protein, progestin and adipoQ receptor 11 (PAQR11), which recruits an adenosine diphosphate ribosylation factor 1-containing protein complex that loads cargos into secretory vesicles. PAQR11-dependent secretion of a protease, PLAU, prevents anoikis and initiates autocrine activation of a PLAU receptor/signal transducer and activator of transcription-3-dependent pathway that up-regulates PAQR11 expression, thereby completing a feedforward loop that amplifies prometastatic effector protein secretion. Pharmacologic inhibition of PLAU receptor impairs the growth and metastasis of p53-deficient cancers. Blockade of PAQR11-dependent secretion inhibits immunosuppressive processes in the tumor microenvironment. Thus, Golgi reprogramming by p53 loss is a key driver of hypersecretion in cancer.
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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.