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Setd7 knockdown decreases Nrf2 and Nrf2-target genes expression, and phenethyl isothiocyanate and ursolic acid induce Setd7 expression, which activates the Nrf2/antioxidant response element signaling pathway and protects DNA from oxidative damage.
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Setd7 KD impacted a larger set of genes and caused a higher fold change compared to PEITC treatment. This study offers new insights into the mechanisms of action of the epigenetic modifier Setd7 and the effects of PEITC treatment in PCa cells and enhances our understanding of the potential cancer preventive/treatment effects of isothiocyanate compounds such as PEITC in PCa.
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High SET7 expression is associated with hepatocellular carcinoma progression.
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SET7/9 expression in nonadherent cells isolated from the effluent of peritoneal dialysis (PD) patients. SET7/9 expression was elevated in nonadherent cells isolated from the effluent of PD patients. SET7/9 expression was positively correlated with dialysate/plasma ratio of creatinine in PD patients.
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Methylation at K436 and K595 respectively by Set7 increases the stability and DNA binding ability of Gli3, resulting in an enhancement of Shh signaling activation.
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the methyltransferase Set9 potentiates TGF-beta signaling by targeting Smad7, an inhibitory downstream effector.
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SET9 expression levels were significantly higher in samples from patients with pathological complete remission than in samples from patients with disease recurrence, which indicates that SET9 acts as a tumor suppressor in breast cancer and that its expression may serve as a prognostic marker for malignancy.
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SETD7 plays a critical role in HCC, and its immunohistochemistry signature provides potential clinical significance for personalized prediction of HCC prognosis.
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These findings underscore the role of KMT7 as an important monomethyltransferase regulating HIV transcription through Tat.
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High SET7 expression is associated with breast cancer.
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SET7 was required for GATA1-induced breast tumor angiogenesis and growth in nude mice. GATA1 and SET7 are independent poor prognostic factors in breast cancer.
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SET7/SET9-mediated YY1 methylation was shown to be involved in YY1-regulated gene transcription and cell proliferation.
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These results demonstrate that S...O chalcogen bonds contribute to AdoMet recognition and can enable methyltransferases to distinguish between substrate and product.
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Reduced expression of SET7 is associated with gastric cancer progression.
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study identified a novel locus associated with serum lycopene concentrations and results raise a number of possibilities regarding the nature of the relationship between SETD7 and lycopene, both independently associated with prostate cancer.
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Lysine methylation by SETD7 is important for the fine-tuning of reactive oxygen species signaling through its regulation on pro-inflammatory responses.
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Knock-down of SETD7 causes differentiation defects in human embryonic stem cell including delay in both the silencing of pluripotency-related genes and the induction of differentiation genes.
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Unleashed expression of Mdm2 in cancer patients with diminished expression of Set7/9 is associated with poor survival outcome.
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Based on our results miR-153 inhibits proliferation and suppresses EMT and the invasive potential of ovarian cancer cells through downregulation of SET7 and ZEB2, supporting the pursuit of miR-153 as a potential target for ovarian cancer intervention.
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Findings indicate the regulation of Wnt/beta-catenin signaling and the role of SET domain-containing protein 7/9 (SET7/9) in cancer cells.