ReviewJournal of experimental & clinical cancer research : CR2011
Down-regulation of UHRF1, associated with re-expression of tumor suppressor genes, is a common feature of natural compounds exhibiting anti-cancer properties.
Review in Journal of experimental & clinical cancer research : CR, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.
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Who cites it
63 citing papers in PubMed, 123 citations in OpenAlex.
- Biology of PEST-containing nuclear proteins as potential targets in ovarian cancer (Review).Oncology letters · 2026Review
- A Hybrid compound H93 treats prostate cancer by directly binding UHRF1 and promoting protein dimerization.Communications chemistry · 2025Article
- Discovery and Characterization of Uracil Derivatives Targeting the Set-and-Ring Domain of UHRF1.Journal of chemical information and modeling · 2025Article
- UHRF1-mediated epigenetic reprogramming regulates glycolysis to promote progression of B-cell acute lymphoblastic leukemia.Cell death & disease · 2025Article
- New insights into coordinated regulation of AHR promoter transcription; molecular mechanisms and therapeutic targets.International journal of biological sciences · 2025Review
- Regulation of PEST-containing nuclear proteins in cancer cells: implications for cancer biology and therapy.Frontiers in oncology · 2025Review
- DiPRO1 distinctly reprograms muscle and mesenchymal cancer cells.EMBO molecular medicine · 2024Article
- Roles of post-translational modifications of UHRF1 in cancer.Epigenetics & chromatin · 2024Review
- Anticancer Drug Discovery Based on Natural Products: From Computational Approaches to Clinical Studies.Biomedicines · 2024Review
- Mechanistic insights into UHRF1‑mediated DNA methylation by structure‑based functional clarification of UHRF1 domains (Review).Oncology letters · 2023Review
- Downregulation of DNA methylation enhances differentiation of THP-1 cells and induces M1 polarization of differentiated macrophages.Scientific reports · 2023Article
- Regulation of UHRF1 acetylation by TIP60 is important for colon cancer cell proliferation.Genes & genomics · 2022Article
- An Insight into Molecular Targets of Breast Cancer Brain Metastasis.International journal of molecular sciences · 2022Review
- The Potential Role ofMolecules (Basel, Switzerland) · 2022Article
- Interfering with the Expression of Ubiquitin-Like with PHD and Ring Finger Domains 1 Can Inhibit the Invasion of Human Renal Cell Carcinoma.Computational and mathematical methods in medicine · 2022Article
- Review
- TIP60 governs the auto‑ubiquitination of UHRF1 through USP7 dissociation from the UHRF1/USP7 complex.International journal of oncology · 2021Article
- Review
- UHRF1 Induces Methylation of theMolecules and cells · 2021Article
- Article
3 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Over-expressed in numerous cancers, Ubiquitin-like containing PHD Ring Finger 1 (UHRF1, also known as ICBP90 or Np95) is characterized by a SRA domain (Set and Ring Associated) which is found only in the UHRF family. UHRF1 constitutes a complex with histone deacetylase 1 (HDAC1) and DNA methyltransferase 1 (DNMT1) via its SRA domain and represses the expression of several tumour suppressor genes (TSGs) including p16INK4A, hMLH1, BRCA1 and RB1. Conversely, UHRF1 is regulated by other TSGs such as p53 and p73. UHRF1 is hypothetically involved in a macro-molecular protein complex called "ECREM" for "Epigenetic Code Replication Machinery". This complex would be able to duplicate the epigenetic code by acting at the DNA replication fork and by activating the right enzymatic activity at the right moment. There are increasing evidence that UHRF1 is the conductor of this replication process by ensuring the crosstalk between DNA methylation and histone modifications via the SRA and Tandem Tudor Domains, respectively. This cross-talk allows cancer cells to maintain the repression of TSGs during cell proliferation. Several studies showed that down-regulation of UHRF1 expression in cancer cells by natural pharmacological active compounds, favors enhanced expression or re-expression of TSGs, suppresses cell growth and induces apoptosis. This suggests that hindering UHRF1 to exert its role in the duplication of the methylation patterns (DNA + histones) is responsible for inducing apoptosis. In this review, we present UHRF1 expression as a target of several natural products and we discuss their underlying molecular mechanisms and benefits for chemoprevention and chemotherapy.
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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.