ArticleOncotarget2016
Reduced expression of SET7/9, a histone mono-methyltransferase, is associated with gastric cancer progression.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 47 citations in OpenAlex.
- Lysine methyltransferase SETD7 in cancer: functions, molecular mechanisms and therapeutic implications.Molecular biology reports · 2025Review
- SETD7 Dual Role in Disease and Opportunities for Therapeutic Intervention: Current Perspectives.Journal of inflammation research · 2025Review
- CAX-INTERACTING PROTEIN4 depletion causes early lethality and pre-mRNA missplicing in Arabidopsis.Plant physiology · 2024Article
- CXIP4 depletion causes early lethality and pre-mRNA missplicing in Arabidopsis.bioRxiv : the preprint server for biology · 2024Article
- Stratification and prognostic evaluation of breast cancer subtypes defined by obesity-associated genes.Discover oncology · 2024Article
- ACAT2 suppresses the ubiquitination of YAP1 to enhance the proliferation and metastasis ability of gastric cancer via the upregulation of SETD7.Cell death & disease · 2024Article
- Tumor-suppressive functions of protein lysine methyltransferases.Experimental & molecular medicine · 2023Review
- The role of SET domain containing lysine methyltransferase 7 in tumorigenesis and development.Cell cycle (Georgetown, Tex.) · 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
- The Epigenetic Regulation of Nonhistone Proteins by SETD7: New Targets in Cancer.Frontiers in genetics · 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
- Expression pattern of histone lysine-specific demethylase 6B in gastric cancer.Oncology letters · 2021Article
- Bcl2l10 induces metabolic alterations in ovarian cancer cells by regulating the TCA cycle enzymes SDHD and IDH1.Oncology reports · 2021Article
- MicroRNAs overexpressed in Crohn's disease and their interactions with mechanisms of epigenetic regulation explain novel aspects of Crohn's disease pathogenesis.Clinical epigenetics · 2021Review
- Sulforaphane and iberin are potent epigenetic modulators of histone acetylation and methylation in malignant melanoma.European journal of nutrition · 2021Article
- p53-Independent Effects of Set7/9 Lysine Methyltransferase on Metabolism of Non-Small Cell Lung Cancer Cells.Frontiers in oncology · 2021Article
- Allyl isothiocyanate regulates lysine acetylation and methylation marks in an experimental model of malignant melanoma.European journal of nutrition · 2020Article
Corrections and comments
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Authors and funding
15 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
SET7/9, a histone methyltransferase, has two distinct functions for lysine methylation. SET7/9 methylates non-histone proteins, such as p53, and participates in their posttranslational modifications. Although SET7/9 transcriptionally activate the genes via H3K4 mono-methylation, its target genes are poorly understood. To clarify whether or not SET7/9 is related to carcinogenesis, we studied alterations of SET7/9 in gastric cancers (GCs). Among the 376 primary GCs, 129 cases (34.3%) showed loss or weak expression of SET7/9 protein compared to matched non-cancerous tissues by immunohistochemistry. Reduced SET7/9 expression was significantly correlated with clinical aggressiveness and worse prognosis. Knockdown of SET7/9 in GC cells markedly increased cell proliferation, migration and invasion. Expression of SREK1IP1, PGC and CCDC28B were inhibited in GC cells with SET7/9 knockdown, while matrix metalloproteinase genes (MMP1, MMP7 and MMP9) were activated. SET7/9 bound and mono-methylated H3K4 at the region of the approximately 4-6 kb upstream from the SREK1IP1 transcriptional start site and the promoters of PGC and CDC28B. Cell proliferation, migration and invasion, and expression of three MMPs were increased in GC cells with SREK1IP knockdown, which were similar to those of SET7/9 knockdown. These data suggest that SET7/9 has tumor suppressor functions, and loss of SET7/9 may contribute to gastric cancer progression.
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