ArticleOncotarget2016
Oncogenic roles of the SETDB2 histone methyltransferase in gastric cancer.
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.
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Who cites it
24 citing papers in PubMed, 27 citations in OpenAlex.
- The anticancer potential of Origanum onites L. in gastric cancer through epigenetic alterations.BMC complementary medicine and therapies · 2025Article
- Histone H3K9 Methylation Is Differentially Modified in Odontogenic Cyst and Tumors.European journal of dentistry · 2025Article
- Prognostic Role of SETDB2 in Clear Cell Renal Cell Carcinoma: Linking Immune Infiltration, Cuproptosis, and Tumor Suppression.Cancer management and research · 2025Article
- Gastric Cancer in the Era of Epigenetics.International journal of molecular sciences · 2024Review
- SETDB2 interacts with BUBR1 to induce accurate chromosome segregation independently of its histone methyltransferase activity.FEBS open bio · 2024Article
- Review
- Gastric cancer: An epigenetic view.World journal of gastrointestinal oncology · 2022Review
- Genomic characterization of intracranial teratomas using whole genome sequencing.Frontiers in oncology · 2022Article
- A metabolism-related gene signature for predicting the prognosis and therapeutic responses in patients with hepatocellular carcinoma.Annals of translational medicine · 2021Article
- Insight into the multi-faceted role of the SUV family of H3K9 methyltransferases in carcinogenesis and cancer progression.Biochimica et biophysica acta. Reviews on cancer · 2021Review
- DNA Methylation Profiling of hTERT Gene Alongside with the Telomere Performance in Gastric Adenocarcinoma.Journal of gastrointestinal cancer · 2020Review
- SETDB2 promoted breast cancer stem cell maintenance by interaction with and stabilization of ΔNp63α protein.International journal of biological sciences · 2020Article
- Oncogenic Roles Of A Histone Methyltransferase SETDB2 In AML1-ETO Positive AML.Cancer management and research · 2020Article
- The Emerging Roles of Heterochromatin in Cell Migration.Frontiers in cell and developmental biology · 2020Review
- Genome Resequencing Reveals Congenital Causes of Embryo and Nestling Death in Crested Ibis (Nipponia nippon).Genome biology and evolution · 2019Article
- Profiling of Epigenetic Features in Clinical Samples Reveals Novel Widespread Changes in Cancer.Cancers · 2019Article
- Emerging roles of H3K9me3, SETDB1 and SETDB2 in therapy-induced cellular reprogramming.Clinical epigenetics · 2019Review
- Integrated Analysis of Genetic Abnormalities of the Histone Lysine Methyltransferases in Prostate Cancer.Medical science monitor : international medical journal of experimental and clinical research · 2019Article
- The molecular landscape of histone lysine methyltransferases and demethylases in non-small cell lung cancer.International journal of medical sciences · 2019Article
- DNA Methylation Readers and Cancer: Mechanistic and Therapeutic Applications.Frontiers in oncology · 2019Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
SETDB2 is a histone H3 lysine 9 (H3K9) tri-methyltransferase that is involved in transcriptional gene silencing. Since it is still unknown whether SETDB2 is linked to carcinogenesis, we studied alterations and functions of SETDB2 in human gastric cancers (GCs). SETDB2 protein was highly expressed in 30 of 72 (41.7%) primary GC tissues compared with their normal counterparts by immunohistochemistry. SETDB2 overexpression was significantly associated with the late stage of GCs (P<0.05) and poor prognosis of GC patients (P<0.05). The GC cell lines with SETDB2 knockdown and overexpression significantly decreased and increased cell proliferation, migration and invasion, respectively (P<0.05). Knockdown of SETDB2 in MKN74 and MKN45 cells reduced global H3K9 tri-methylation (me3) levels. Microarray analysis indicated that expression of WWOX and CADM1, tumor suppressor genes, was significantly enhanced in MKN74 cells after SETDB2 knockdown. Chromatin immunoprecipitation assays showed that the H3K9me3 levels at the promoter regions of these two genes corresponded to the SETDB2 expression levels in GC cells. Moreover, ectopic SETDB2 protein was recruited to their promoter regions. Our data suggest that SETDB2 is associated with transcriptional repression of WWOX and CADM1, and hence overexpression of SETDB2 may contribute to GC progression.
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