ArticleBritish journal of cancer2021
CREPT/RPRD1B promotes tumorigenesis through STAT3-driven gene transcription in a p300-dependent manner.
Article in British journal of cancer, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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15 citing papers in PubMed, 22 citations in OpenAlex.
- Targeting RPRD1B overcomes chemoresistance in gastric cancer by suppressing the TOPBP1-mediated DNA damage repair pathway.Cellular oncology (Dordrecht, Netherlands) · 2026Article
- Downregulation of RORl via STAT3 and P300 Promotes P38 Pathway- Dependent Lens Epithelial Cells Apoptosis in Age-Related Cataract.Biochemical genetics · 2026Article
- Comprehensive pan-cancer analysis of RPRD1B as a promising diagnostic and prognostic biomarker.Discover oncology · 2026Article
- Review
- Antisense oligonucleotides targeting IRF4 alleviate psoriasis.Acta pharmaceutica Sinica. B · 2025Article
- CREPT is required for the metastasis of triple-negative breast cancer through a co-operational-chromatin loop-based gene regulation.Molecular cancer · 2025Article
- CREPT promotes LUAD progression by enhancing the CDK9 and RNAPII assembly to promote ERK-driven gene transcription.Theranostics · 2025Article
- Article
- Exosome-derived circ-001422 promotes tumor-associated macrophage M2 polarization to accelerate the progression of glioma.Communications biology · 2024Article
- Roles of lncRNAs in NF-κB-Mediated Macrophage Inflammation and Their Implications in the Pathogenesis of Human Diseases.International journal of molecular sciences · 2024Review
- Microenvironment-induced CREPT expression by cancer-derived small extracellular vesicles primes field cancerization.Theranostics · 2024Article
- IL-17 induces NSCLC cell migration and invasion by elevating MMP19 gene transcription and expression through the interaction of p300-dependent STAT3-K631 acetylation and its Y705-phosphorylation.Oncology research · 2024Article
- Inhibition of STAT3 phosphorylation by colchicine regulates NLRP3 activation to alleviate sepsis-induced acute lung injury.Inflammopharmacology · 2023Article
- Multifunctional Roles of Betulinic Acid in Cancer Chemoprevention: Spotlight on JAK/STAT, VEGF, EGF/EGFR, TRAIL/TRAIL-R, AKT/mTOR and Non-Coding RNAs in the Inhibition of Carcinogenesis and Metastasis.Molecules (Basel, Switzerland) · 2022Review
- CREPT Disarms the Inhibitory Activity of HDAC1 on Oncogene Expression to Promote Tumorigenesis.Cancers · 2022Article
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Authors and funding
16 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundSignal transducer and activator of transcription 3 (STAT3) has been shown to upregulate gene transcription during tumorigenesis. However, how STAT3 initiates transcription remains to be exploited. This study is to reveal the role of CREPT (cell cycle-related and elevated-expression protein in tumours, or RPRD1B) in promoting STAT3 transcriptional activity.
methodsBALB/c nude mice, CREPT overexpression or deletion cells were employed for the assay of tumour formation, chromatin immunoprecipitation, assay for transposase-accessible chromatin using sequencing.
resultsWe demonstrate that CREPT, a recently identified oncoprotein, enhances STAT3 transcriptional activity to promote tumorigenesis. CREPT expression is positively correlated with activation of STAT3 signalling in tumours. Deletion of CREPT led to a decrease, but overexpression of CREPT resulted in an increase, in STAT3-initiated tumour cell proliferation, colony formation and tumour growth. Mechanistically, CREPT interacts with phosphorylated STAT3 (p-STAT3) and facilitates p-STAT3 to recruit p300 to occupy at the promoters of STAT3-targeted genes. Therefore, CREPT and STAT3 coordinately facilitate p300-mediated acetylation of histone 3 (H3K18ac and H3K27ac), further augmenting RNA polymerase II recruitment. Accordingly, depletion of p300 abolished CREPT-enhanced STAT3 transcriptional activity.
conclusionsWe propose that CREPT is a co-activator of STAT3 for recruiting p300. Our study provides an alternative strategy for the therapy of cancers related to STAT3.
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