ArticleJournal of Cancer2017
Opposite Effects of SET7/9 on Apoptosis of Human Acute Myeloid Leukemia Cells and Lung Cancer Cells.
Article in Journal of Cancer, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
15 citing papers in PubMed, 23 citations in OpenAlex.
- Oxidative stress and its related epigenetic modifications in vascular calcification: mechanisms and advances.Frontiers in cardiovascular medicine · 2025Review
- SETD7 Dual Role in Disease and Opportunities for Therapeutic Intervention: Current Perspectives.Journal of inflammation research · 2025Review
- Dysregulation of histone modifications in bone marrow mesenchymal stem cells during skeletal ageing: roles and therapeutic prospects.Stem cell research & therapy · 2023Review
- [Research Progress of Role and Mechanism of SETD7 in Tumor Occurrence and Progression].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2023Article
- A Systematic Review to Define the Multi-Faceted Role of Lysine Methyltransferase SETD7 in Cancer.Cancers · 2022Review
- How Protein Methylation Regulates Steroid Receptor Function.Endocrine reviews · 2022Review
- Oncogene or Tumor Suppressor: The Coordinative Role of Lysine Methyltransferase SET7/9 in Cancer Development and the Related Mechanisms.Journal of Cancer · 2022Review
- Benzyl and phenethyl isothiocyanates as promising epigenetic drug compounds by modulating histone acetylation and methylation marks in malignant melanoma.Investigational new drugs · 2021Article
- Review
- Sulforaphane and iberin are potent epigenetic modulators of histone acetylation and methylation in malignant melanoma.European journal of nutrition · 2021Article
- MiR-345-5p inhibits tumorigenesis of papillary thyroid carcinoma by targeting SETD7.Archives of medical science : AMS · 2020Article
- SET7 interacts with HDAC6 and suppresses the development of colon cancer through inactivation of HDAC6.American journal of translational research · 2020Article
- SET7/9 promotes hepatocellular carcinoma progression through regulation of E2F1.Oncology reports · 2018Article
- Deciphering the Epigenetic Symphony of Cancer: Insights and Epigenetic Therapies Implications.Technology in cancer research & treatmentReview
- Targeting epigenetic regulators for cancer therapy: mechanisms and advances in clinical trials.Signal transduction and targeted therapyReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
SET7/9 is a protein lysine methyltransferases (PLMTs or PKMTs) which methylates both histone H3K4 and non-histone proteins including transcriptional factors, tumor suppressors, and membrane-associated receptors. Methylation of these proteins alters protein activity and leads to changes in cellular behavior and a series of biological processes. This study aims to investigate the role of SET7/9 in human acute myeloid leukemia (AML) and non-small-cell lung cancer (NSCLC). We examined the expression of SET7/9 in AML cells and NSCLC cells and detected the methylation status of the SET7/9 promoter region. To evaluate the effect of SET7/9 expression changes on cell apoptosis, cell apoptosis rates were determined after SET7/9 overexpression or down-regulation. Our results showed that SET7/9 induces apoptosis of AML cells and inhibits apoptosis of NSCLC cells, suggesting differential effects of SET7/9 on cellular apoptosis and carcinogenesis depending on different cancer types and genetic contexts. Furthermore, we also demonstrated that SET7/9 suppresses cell apoptosis via modulation of E2F1 under circumstance of p53 deficiency in NSCLC cells.
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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.