ArticleJournal of cancer science & therapy2013
SET domain-containing Protein 4 (SETD4) is a Newly Identified Cytosolic and Nuclear Lysine Methyltransferase involved in Breast Cancer Cell Proliferation.
Article in Journal of cancer science & therapy, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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
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Who cites it
21 citing papers in PubMed, 46 citations in OpenAlex.
- SETD4 as a marker of disease burden and treatment response in childhood acute lymphoblastic leukemiaOncology letters · 2026Article
- The emerging paradigms of SETD family enzymes as epigenetic regulators of the immune response in inflammatory diseases.Frontiers in immunology · 2026Review
- Identification of SETD4 as an Onco-Immunological Biomarker Encompassing the Tumor Microenvironment, Prognoses, and Therapeutic Responses in Various Human Cancers.Immunity, inflammation and disease · 2025Article
- An extract from the frass of swallowtail butterfly (Papilio machaon) larvae inhibits HCT116 colon cancer cell proliferation but not other cancer cell types.BMC genomics · 2023Article
- TBK1-stabilized ZNF268a recruits SETD4 to methylate TBK1 for efficient interferon signaling.The Journal of biological chemistry · 2023Article
- Methyltransferases: Functions and Applications.Chembiochem : a European journal of chemical biology · 2022Review
- SETD4 cells contribute to brain development and maintain adult stem cell reservoir for neurogenesis.Stem cell reports · 2022Article
- SETD4-mediated KU70 methylation suppresses apoptosis.Cell reports · 2022Article
- Protein methylation in mitochondria.The Journal of biological chemistry · 2022Review
- Nonhistone Lysine Methylation as a Protein Degradation Signal.Journal of chemistry · 2022Article
- SETD4 in the Proliferation, Migration, Angiogenesis, Myogenic Differentiation and Genomic Methylation of Bone Marrow Mesenchymal Stem Cells.Stem cell reviews and reports · 2021Article
- Somatic Functional Deletions of Upstream Open Reading Frame-Associated Initiation and Termination Codons in Human Cancer.Biomedicines · 2021Article
- Identification of a localized nonsense-mediated decay pathway at the endoplasmic reticulum.Genes & development · 2020Article
- Deletion of Mouse Setd4 Promotes the Recovery of Hematopoietic Failure.International journal of radiation oncology, biology, physics · 2020Article
- Loss of Setd4 delays radiation-induced thymic lymphoma in mice.DNA repair · 2020Article
- SET domain containing protein 5 (SETD5) enhances tumor cell invasion and is associated with a poor prognosis in non-small cell lung cancer patients.BMC cancer · 2019Article
- MiR-202 controls female fecundity by regulating medaka oogenesis.PLoS genetics · 2018Article
- Human METTL12 is a mitochondrial methyltransferase that modifies citrate synthase.FEBS letters · 2017Article
- SETD4 Regulates Cell Quiescence and Catalyzes the Trimethylation of H4K20 during Diapause Formation in Artemia.Molecular and cellular biology · 2017Article
- Pharmacogenomic Characterization and Isobologram Analysis of the Combination of Ascorbic Acid and Curcumin-Two Main Metabolites ofFrontiers in pharmacology · 2017Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
Cancer is comprised of a multitude of epigenetic abnormalities, including the global loss and regional gain of DNA methylation as well as alterations in histone methylation. Here, we characterize a new methyltransferase, SET domain-containing protein 4 (SETD4), which is involved in breast carcinogenesis. Quantitative real-time PCR (qPCR) showed elevated expression levels of SETD4 in several breast cancer cell lines. SETD4 overexpression was confirmed by western blot analysis suggesting a correlation between high expression of SETD4 and a lack of the estrogen receptor (ER) in breast cancer. In addition, cell fractionation studies and confocal immunofluorescence revealed the nuclear and non-nuclear localization of this new protein. SETD4 knockdown in breast cancer cell lines significantly suppressed their proliferation and delayed the G1/S cell cycle transition without affecting apoptosis. Furthermore, western blot analysis showed that knockdown of SETD4 decreased cyclin D1 expression, revealing the involvement of SETD4 in cell cycle regulation. These data imply that SETD4 plays a crucial role in breast carcinogenesis and could be a novel molecular target for the development of new strategies for the diagnosis and treatment of breast cancer.
Identifiers
24738023PMC3984760W2012016144What OpenQuestion 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 OpenQuestion graph.