ArticleOncotarget2016
Setdb1, a novel interactor of ΔNp63, is involved in breast tumorigenesis.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
24 citing papers in PubMed, 43 citations in OpenAlex.
- SETDB1 amplification in osteosarcomas: Insights from its role in healthy tissues and other cancer types.Oncotarget · 2025Review
- ΔNp63 bookmarks and creates an accessible epigenetic environment for TGFβ-induced cancer cell stemness and invasiveness.Cell communication and signaling : CCS · 2024Article
- SETDB1 as a cancer target: challenges and perspectives in drug design.RSC medicinal chemistry · 2024Review
- Cytoplasmic localization of SETDB1‑induced Warburg effect via c‑MYC‑LDHA axis enhances migration and invasion in breast carcinoma.International journal of molecular medicine · 2024Article
- SETDB1 tumour suppressor roles in near-haploid mesothelioma involve TP53.British journal of cancer · 2023Article
- EZH2 regulates a SETDB1/ΔNp63α axis via RUNX3 to drive a cancer stem cell phenotype in squamous cell carcinoma.Oncogene · 2022Article
- ΔNp63-Senataxin circuit controls keratinocyte differentiation by promoting the transcriptional termination of epidermal genes.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Histone Methyltransferase SETDB1 Promotes Immune Evasion in Colorectal CancerJournal of immunology research · 2022Article
- Structure, Activity and Function of the SETDB1 Protein Methyltransferase.Life (Basel, Switzerland) · 2021Review
- New immunological potential markers for triple negative breast cancer: IL18R1, CD53, TRIM, Jaw1, LTB, PTPRCAP.Discover oncology · 2021Article
- Prominent Role of Histone Modifications in the Regulation of Tumor Metastasis.International journal of molecular sciences · 2021Review
- SETDB1 in cancer: overexpression and its therapeutic implications.American journal of cancer research · 2021Review
- Review
- SETDB1 Overexpression Sets an Intertumoral Transcriptomic Divergence in Non-small Cell Lung Carcinoma.Frontiers in genetics · 2020Article
- SETDB2 promoted breast cancer stem cell maintenance by interaction with and stabilization of ΔNp63α protein.International journal of biological sciences · 2020Article
- Increased Expression of FosB through Reactive Oxygen Species Accumulation Functions as Pro-Apoptotic Protein in Piperlongumine Treated MCF7 Breast Cancer Cells.Molecules and cells · 2019Article
- p63 at the Crossroads between Stemness and Metastasis in Breast Cancer.International journal of molecular sciences · 2019Review
- ΔNp63 in squamous cell carcinoma: defining the oncogenic routes affecting epigenetic landscape and tumour microenvironment.Molecular oncology · 2019Review
- LncRNA FENDRR represses proliferation, migration and invasion through suppression of survivin in cholangiocarcinoma cells.Cell cycle (Georgetown, Tex.) · 2019Article
- SETDB1 regulates SMAD7 expression for breast cancer metastasis.BMB reports · 2019Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
ΔNp63 has been recently involved in self-renewal potential of breast cancer stem cells. Although the p63 transcriptional profile has been extensively characterized, our knowledge of the p63-binding partners potentially involved in the regulation of breast tumour progression is limited. Here, we performed the yeast two hybrid approach to identify p63α interactors involved in breast tumorigenesis and we found that SETDB1, a histone lysine methyl transferases, interacts with ΔNp63α and that this interaction contributes to p63 protein stability. SETDB1 is often amplified in primary breast tumours, and its depletion confers to breast cancer cells growth disadvantage. We identified a list of thirty genes repressed by ΔNp63 in a SETDB1-dependent manner, whose expression is positively correlated to survival of breast cancer patients. These results suggest that p63 and SETDB1 expression, together with the repressed genes, may have diagnostic and prognostic potential.
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What Socratic holds
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 Socratic graph.