EC Number   |
Application |
Reference |
|---|
   2.1.1.366 | medicine |
expression of an inactivated form of SETDB1 in human pancreatic ductal adenocarcinoma cells with wild-type TP53 results in TP53-induced apoptosis |
759292 |
| 2.1.1.366 | medicine |
loss of SETDB1 from pancreas accelerates formation of premalignant lesions in mice with pancreata that express activated KRAS. Expression of genes in the apoptotic pathway is upregulated and genes are regulated by p53 in SETDB1-deficient pancreata. Deletion of Setdb1 from pancreas prevents formation of pancreatic ductal adenocarcinoma, concomitant with increased apoptosis and upregulated expression of Trp53 in mice heterozygous for disruption of Trp53. Pancreata of mice with homozygous disruption of Trp53 have no increased apoptosis, and pancreatic ductal adenocarcinomas develop. SETDB1 binds to the Trp53 promoter to regulate its expression |
759292 |
| 2.1.1.366 | medicine |
overexpression of SETDB1 contributes to melanoma tumorigenesis. SETDB1 is highly amplified in melanoma cells and in the patient tumors. Increased expression of SETDB1 correlates with SETDB1 amplification and is associated with a more aggressive phenotype in in vitro and in vivo studies. SETDB1 implements its effects via regulation of thrombospondin 1, and the SET-domain of SETDB1 is essential for the maintenance of its tumorigenic activity. Inhibition of SETDB1 reduces cell growth in melanomas resistant to targeted treatments |
759353 |
| 2.1.1.366 | medicine |
overexpression of SETDB1 contributes to melanoma tumorigenesis. SETDB1 is highly amplified in melanoma cells. Increased expression of SETDB1 correlates with SETDB1 amplification and is associated with a more aggressive phenotype in in vitro and in vivo studies. SETDB1 implements its effects via regulation of thrombospondin 1, and the SET-domain of SETDB1 is essential for the maintenance of its tumorigenic activity. Inhibition of SETDB1 reduces cell growth in melanomas resistant to targeted treatments |
759353 |
| 2.1.1.366 | medicine |
SETDB1 depletion effectively converts stem-like colorectal cancer cells into postmitotic cells and restores normal morphology in patient-derived colorectal cancer organoids. SETDB1 depletion recapitulates global gene expression profiles of normal differentiated cells by restoring the transcriptional activity of core transcription factors such as CDX2, ELF3, HNF4G, PPARG, and VDR, on their target genes |
759760 |
| 2.1.1.366 | medicine |
SETDB1 expression is highly amplified in colorectal cancer. SETDB1 downregulation in SW480 and HCT116 cells reduces cell proliferation, migration, invasion, and increased colorectal cancer cells apoptosis. SETDB1 overexpression promotes colorectal cancer cells proliferation, migration, and invasion. High expression of SETDB1 is associated with a more aggressive phenotype in vitro. Cell cycle is arrested in G1 phase after SETDB1 silencing. Depletion of SETDB1 in vivo suppresses colorectal cancer cells proliferation. p21 is the target of SETDB1. After transfection with siSETDB1, expression of p21 s distinctly increased. Expression of p21 is significantly decreased after overexpression of SETDB1. SETDB1 can bind to the promoter of p21 and regulate its H3K9me3 enrichment level. Silencing of SETDB1 inhibits colorectal cancer tumorigenesis in vivo |
759019 |
| 2.1.1.366 | medicine |
Setdb1 has a constant role in endogenous retrovirus silencing. Distinctive sets of endogenous retroviruses are reactivated in different types of Setdb1-deficient somatic cells, including the VL30-class of endogenous retroviruses in mouse embryonic fibroblasts. A viral defense response is induced in immortalized Setdb1 knock-out embryonic fibroblasts |
759835 |
