ArticleCell reports2015
Disruption of the PHRF1 Tumor Suppressor Network by PML-RARα Drives Acute Promyelocytic Leukemia Pathogenesis.
Article in Cell reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
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Who cites it
16 citing papers in PubMed, 21 citations in OpenAlex.
- Histone H3 N-terminal recognition by the PHD finger of PHRF1 is required for proper DNA damage response.Nucleic acids research · 2025Article
- A novel mesothelioma molecular classification based on malignant cell differentiation.Cancer cell international · 2025Article
- Mono-ubiquitination of TopBP1 by PHRF1 enhances ATR activation and genomic stability.Nucleic acids research · 2025Article
- Clinicopathologic and proteomic characteristics of low-grade undifferentiated spindle cell sarcoma.Frontiers in molecular biosciences · 2025Article
- Cellular hierarchy insights reveal leukemic stem-like cells and early death risk in acute promyelocytic leukemia.Nature communications · 2024Article
- Article
- A novel network pharmacology approach for leukaemia differentiation therapy using MogrifyOncogene · 2022Article
- An important role of PHRF1 in dendritic architecture and memory formation by modulating TGF-β signaling.Scientific reports · 2020Article
- Characterization of the plant homeodomain (PHD) reader family for their histone tail interactions.Epigenetics & chromatin · 2020Article
- TGIF1-Twist1 axis in pancreatic ductal adenocarcinoma.Computational and structural biotechnology journal · 2020Review
- Article
- TGIF1 functions as a tumor suppressor in pancreatic ductal adenocarcinoma.The EMBO journal · 2019Article
- Acute Promyelocytic Leukemia: A History over 60 Years-From the Most Malignant to the most Curable Form of Acute Leukemia.Oncology and therapy · 2019Review
- Functional analysis of Cullin 3 E3 ligases in tumorigenesis.Biochimica et biophysica acta. Reviews on cancer · 2018Review
- All-trans retinoic acid and arsenic trioxide fail to derepress the monocytic differentiation driver Irf8 in acute promyelocytic leukemia cells.Cell death & disease · 2017Article
- Overexpression of PHRF1 attenuates the proliferation and tumorigenicity of non-small cell lung cancer cells.Oncotarget · 2016Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
PHRF1 functions as an essential component of the TGF-β tumor suppressor pathway by triggering degradation of the homeodomain repressor factor TGIF. This leads to redistribution of cPML into the cytoplasm, where it coordinates phosphorylation and activation of Smad2 by the TGF-β receptor. In acute promyelocytic leukemia (APL), acquisition of PML-RARα is known to impede critical aspects of TGF-β signaling, including myeloid differentiation. Although these defects are thought to rely on suppression of cPML activity, the mechanisms underlying this phenomenon remain enigmatic. Here, we find that an abnormal function of PML-RARα is to interfere with TGIF breakdown, presumably by competing with PHRF1 for binding to TGIF, culminating in cPML sequestration and inactivation. Enforcing PHRF1 activity is sufficient to restore TGF-β cytostatic signaling in human blasts and suppress APL formation in a mouse model of APL, providing proof-of-concept data that suppression of PHRF1 activity by PML-RARα represents a critical determinant in APL pathogenesis.
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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.