ArticleCell death & disease2020
SETDB1 promotes the progression of colorectal cancer via epigenetically silencing p21 expression.
Article in Cell death & disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 46 citations in OpenAlex.
- Dynamic regulation of H3K9 modifications in cancer: pathogenesis and targeted therapies.Biomarker research · 2026Review
- SETDB1 cooperates with the CRL4B complex to promote colorectal cancer tumorigenesis by disrupting circadian rhythm.Oncogene · 2026Article
- Beyond hypoxia and ccRCC: the expanding universe of VHL novel targets and next-generation therapeutics.Biomarker research · 2026Review
- ITGB5 promotes immune escape in hepatocellular carcinoma by regulating PD-L1 through SETDB1/Hippo signaling pathway.Cellular oncology (Dordrecht, Netherlands) · 2026Article
- SETDB1 induces H3K9me3 methylation modification of RASSF2 to inhibit PTEN and facilitate ovarian cancer progression.Molecular genetics and genomics : MGG · 2026Article
- The SUMO specific peptidase SENP3 promotes papillary thyroid cancer progression by deSUMOylation of SETDB1 and regulating GLI2 transcription.Clinical and experimental medicine · 2026Article
- In Vitro Cell Viability and Migration Inhibitory Effects of Isorhamnetin in Non-Small Cell Lung Cancer Cells.Biomedicines · 2026Article
- SETDB1 promotes gastric cancer progression via UPR and mTOR pathway.Cancer cell international · 2026Article
- The epigenetic regulator SETDB1 as a key component of cancer stem cells and drug resistance in primary liver cancer.Cellular oncology (Dordrecht, Netherlands) · 2026Article
- DNA, RNA, and histone methylation regulation enzymes and their crosstalk in colorectal carcinogenesis and progression: a review of molecular mechanisms, clinical implications, and future perspectives.Cellular & molecular biology letters · 2025Review
- Functional Roles and Mechanistic Insights of YEATS Domain Proteins in Digestive System Tumors.Digestive diseases and sciences · 2025Review
- Identification and clinical implications of endogenous retrovirus elements suppressed by SETDB1 in hepatocellular carcinoma.JHEP reports : innovation in hepatology · 2025Article
- SETDB1 amplification in osteosarcomas: Insights from its role in healthy tissues and other cancer types.Oncotarget · 2025Review
- Targeting the Tumor Epigenetic Regulator SETDB1 for Tumor Therapy.Current cancer drug targets · 2025Review
- Disrupting CENP-N mediated SEPT9 methylation as a strategy to inhibit aerobic glycolysis and liver metastasis in colorectal cancer.Clinical & experimental metastasis · 2024Article
- SETDB1 targeting SESN2 regulates mitochondrial damage and oxidative stress in renal ischemia-reperfusion injury.BMC biology · 2024Article
- The epigenetic landscape in intestinal stem cells and its deregulation in colorectal cancer.Stem cells (Dayton, Ohio) · 2024Review
- SETDB1 as a cancer target: challenges and perspectives in drug design.RSC medicinal chemistry · 2024Review
- SETDB1 promotes progression through upregulation of SF3B4 expression and regulates the immunity in ovarian cancer.Journal of ovarian research · 2024Article
- The functions of SET domain bifurcated histone lysine methyltransferase 1 (SETDB1) in biological process and disease.Epigenetics & chromatin · 2023Review
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
SETDB1, a histone H3K9 methyltransferase, has been reported to be upregulated in a variety of tumors and promotes cancer development. However, the exact pathogenesis of SETDB1 in human colorectal cancer (CRC) is hitherto unknown. Here, we showed that SETDB1 expression was highly amplified in CRC. Functionally, SETDB1 downregulation in SW480 and HCT116 cells reduced cell proliferation, migration, invasion, and increased CRC cells apoptosis. In contrast, SETDB1 overexpression promoted CRC cells proliferation, migration, and invasion. High expression of SETDB1 was associated with a more aggressive phenotype in vitro. Flow cytometry showed that cell cycle was arrested in G1 phase after SETDB1 silencing. Furthermore, depletion of SETDB1 in vivo suppressed CRC cells proliferation. Mechanistically, p21 was identified as the target of SETDB1. After transfected with siSETDB1, expression of p21 was distinctly increased. In contrast, expression of p21 was significantly decreased after overexpression SETDB1. We also showed that SETDB1 could be involved in the regulation of epithelial-mesenchymal transition (EMT) in HCT116 cells. Moreover, we confirmed that SETDB1 could regulate the activity of p21 promoter by dual-luciferase repoter assay, and proved that SETDB1 could bind to the promoter of p21 and regulate its H3K9me3 enrichment level by ChIP-PCR experiment. Finally, we verified that silencing of SETDB1 inhibited CRC tumorigenesis in vivo. In conclusion, our results indicate that SETDB1 is a major driver of CRC development and might provide a new therapeutic target for the clinical treatment of CRC.
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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.