ArticleDevelopmental cell2017
Tumor-Suppressor Inactivation of GDF11 Occurs by Precursor Sequestration in Triple-Negative Breast Cancer.
Article in Developmental cell, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.
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Who cites it
60 citing papers in PubMed, 93 citations in OpenAlex.
- GDF11 upregulation independently predicts shorter overall-survival of uveal melanoma.PloS one · 2019Trial
- In vivo CRISPR screening links NFKB1 to endocrine resistance in ER+ breast cancer.Endocrine-related cancer · 2026Article
- PCSK5 promotes angiogenesis and cardiac repair after myocardial infarction.Nature communications · 2026Article
- Identification and functional validation of EPS15L1 as a key driver of triple-negative breast cancer.NPJ breast cancer · 2026Article
- Tumor-derived GDF15 induces CCN3⁺ Schwann cells to promote cancer pain in pancreatic cancer.Nature communications · 2026Article
- TGFβ signaling systems are prone to inhibition and ligand competition by coreceptor.bioRxiv : the preprint server for biology · 2026Article
- PCSK5M452I Is a Recessive Hypomorph Exclusive to MCF10DCIS.com Cells.Molecular cancer research : MCR · 2026Article
- Prognostic value of brown adipocyte-related genes in colorectal cancer: a multi-omics and Mendelian randomization study.Discover oncology · 2025Article
- Single-cell dynamics reveal a stress-induced decision between hypertrophy and apoptosis in neonatal rat cardiomyocytes.Journal of molecular and cellular cardiology plus · 2025Article
- Growth differentiation factor 11 modulates metabolism, mitigating the pro-tumoral behavior provided by M2-like macrophages in hepatocellular carcinoma-derived cells.World journal of gastroenterology · 2025Article
- Single-cell and spatial analyses of the GDF family in tumors, with a focus on the prognostic and biological role of GDF15 in hepatocellular carcinoma.Cell & bioscience · 2025Article
- Comprehensive analysis of GDFs as therapeutic targets and prognosis biomarkers in gastric cancer.Medicine · 2025Article
- GDF11 downregulates FOXP3 in T-cell acute lymphoblastic leukemia-derived cells and associates with restraining aggressiveness.Oncology research · 2025Article
- PCSK5 downregulation promotes the inhibitory effect of andrographolide on glioblastoma through regulating STAT3.Molecular and cellular biochemistry · 2025Article
- Comprehensive Analysis of Prognostic Alternative Splicing Signatures in Tumor Immune Infiltration in Bladder Cancer.Recent patents on anti-cancer drug discovery · 2025Article
- Chemogenetic neuronal silencing decouples c-Jun activation from cell death in the temporal cortex.The European journal of neuroscience · 2024Article
- Proteome-wide copy-number estimation from transcriptomics.Molecular systems biology · 2024Article
- Fibroblast stromal support model for predicting human papillomavirus-associated cancer drug responses.Journal of virology · 2024Article
- GDF11 inhibits the malignant progression of hepatocellular carcinoma via regulation of the mTORC1‑autophagy axis.Experimental and therapeutic medicine · 2024Article
- Lactate in breast cancer cells is associated with evasion of hypoxia-induced cell cycle arrest and adverse patient outcome.Human cell · 2024Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 2 countries.
Funding
Abstract
Triple-negative breast cancer (TNBC) is an aggressive and heterogeneous carcinoma in which various tumor-suppressor genes are lost by mutation, deletion, or silencing. Here we report a tumor-suppressive mode of action for growth-differentiation factor 11 (GDF11) and an unusual mechanism of its inactivation in TNBC. GDF11 promotes an epithelial, anti-invasive phenotype in 3D triple-negative cultures and intraductal xenografts by sustaining expression of E-cadherin and inhibitor of differentiation 2 (ID2). Surprisingly, clinical TNBCs retain the GDF11 locus and expression of the protein itself. GDF11 bioactivity is instead lost because of deficiencies in its convertase, proprotein convertase subtilisin/kexin type 5 (PCSK5), causing inactive GDF11 precursor to accumulate intracellularly. PCSK5 reconstitution mobilizes the latent TNBC reservoir of GDF11 in vitro and suppresses triple-negative mammary cancer metastasis to the lung of syngeneic hosts. Intracellular GDF11 retention adds to the concept of tumor-suppressor inactivation and reveals a cell-biological vulnerability for TNBCs lacking therapeutically actionable mutations.
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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.