ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
PJA2 Suppresses Colorectal Cancer Progression by Controlling HDAC2 Degradation and Stability.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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The trial behind it
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Who cites it
7 citing papers in PubMed.
- SPSB1 Promotes Subcutaneous Adipose Hyperplasia in Facial Port-Wine Stains by Controlling HDAC1 Degradation and Stability Through Two Distinct Proteolytic Pathways.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Transcriptome-Wide Cox Regression Identifies Candidate Survival-Associated Genes in Newly Diagnosed Acute Myeloid Leukemia.Cancer informatics · 2026Article
- Butyrate blocks cell cycle progression in colorectal cancer organoids partially through HDAC2 inhibition.Frontiers in immunology · 2026Article
- Deacetylation of ACLY Mediates RNA MAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Clinical Utility of IFIT Proteins in Human Malignancies.Biomedicines · 2025Review
- Histone Deacetylase Inhibitors Promote the Anticancer Activity of Cisplatin: Mechanisms and Potential.Pharmaceuticals (Basel, Switzerland) · 2025Review
- PJA2 Suppresses Colorectal Cancer Progression by Controlling HDAC2 Degradation and Stability.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
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Authors and funding
14 authors.
Funding
Abstract
PJA2 is documented to degrade various substrates. Nevertheless, the role of PJA2 as an E3 ubiquitin-protein ligase in colorectal cancer (CRC) progression remains unexplored. The correlation between PJA2 mRNA levels and clinical characteristics is investigated using data from The Cancer Genome Atlas (TCGA) database. Quantitative real-time polymerase chain reaction (qRT-PCR) and immunohistochemistry (IHC) are utilized to evaluate PJA2 expression levels in CRC tissues. The biological functions of PJA2 are confirmed through colony formation assays and azoxymethane/dextran sulfate sodium (AOM/DSS) mouse model of CRC, among other experimental approaches. The underlying molecular mechanisms of PJA2 action are elucidated using RNA sequencing (RNA-seq), co-immunoprecipitation (co-IP), proximity ligation assay (PLA), and chromatin immunoprecipitation (ChIP). Our research discovered that PJA2 is downregulated in CRC tissues and decreased PJA2 expression correlates with poor prognosis. Functionally, in vivo and in vitro experiments uncovered that PJA2 inhibits tumor cell proliferation and promotes apoptosis. Mechanistically, PJA2 recognized histone deacetylase 2 (HDAC2) via its RING-B-box domain (RBD) and bind to the N-terminal of HDAC2, facilitating ubiquitination at the lysine 90 (K90) residue. PJA2-mediated degradation of HDAC2 counteracts the transcriptional repression of the interferon-induced protein with the tetratricopeptide repeats (IFIT) family, thereby suppressing CRC progression. The data demonstrates that PJA2 suppresses CRC progression through the PJA2/HDAC2/IFIT axis, and its expression is regulated by HDAC2, thus constituting a positive feedback loop. Consequently, PJA2 may serve as a potential therapeutic target for CRC, and interrupting this feedback loop can represent a viable treatment strategy to restrain CRC progression.
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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.