SUV39H1 (SUV39H1 Histone Lysine Methyltransferase)

Parallel analyses in human HNSCC cells overexpressing the H3K36M oncohistone reveal conserved disruptions to the epigenome and chromatin architecture. Together, these results establish H3K36 methylation as a pivotal regulator of chromatin state and genomic structure.

Inhibition of the mTORC1/4E-BP1 signaling pathway, either pharmacologically or genetically, reduces SUV39H1 translation, whereas ectopic SUV39H1 expression restores CSC-like properties and DNA damage even in the presence of pathway inhibition. Together, these findings identify mTORC1/4E-BP1-mediated translational upregulation of SUV39H1 as an important mechanistic link in Cr(VI)-induced carcinogenesis, revealing a novel layer of regulation that integrates translational control with environmental carcinogen-induced epigenetic reprogramming.

Imperatorin ameliorates MAFLD through modulating Suv39h1/Fabps/Cept1 signalling pathway.

SUV39H1 silencing reduced EMT marker genes CDH2, SNAI1 and MARCKS. SUV39H1 has an oncogenic role in pHGG and presents a promising therapeutic target.

SUV39H2 is a novel regulator of GSC maintenance. Dual targeting of SUV39H2 and SUV39H1 May offer a potential therapeutic approach for GBM.

Consequently, SKI deficiency disrupted centromere integrity and resulted in aberrant chromosome segregation, micronuclei formation, and chromosome instability. The identification of SKI as a key participant in the epigenetic-mediated silencing of pericentromeric and ribosomal DNA provides a fundamental insight, paving the way for new research into the intricate relationship between transcriptional regulation and genome instability during cancer progression, and opening novel opportunities for therapeutic intervention.

These enzymes are critical for maintaining the epigenetic landscape essential for effective muscle repair, as they regulate the transition between different myogenic states and ensure coordinated gene expression during regeneration. Here, we present a comprehensive overview of the functions of the SUV39 KMTs family in skeletal muscle biology, emphasizing their role in adult myogenesis and exploring the broader implications for muscle regeneration and related diseases.

miRNA array analysis showed notable and significant reductions in the expression levels of several miRNAs. The results obtained from this comprehensive study are expected to make a significant contribution to the elucidation of ZEA toxicity.

Integrated transcriptomic analysis indicated that HIC1 might regulate VSMC phenotypic modulation by activating Jag1 (Jagged 1) transcription. Our data suggest that Suv39h1 is a novel regulator of vascular injury and targeted for intervention of restenosis.

We further validated the functions of the HELLS-MIEF1 axis by MIEF1 overexpression and mitochondrial fusion drug. Our study has important implications for medical science by highlighting the crosstalk between epigenetics and metabolism through nuclear chromatin remodeler HELLS and mitochondrial protein MIEF1.

H3K9me3-mediated repetitive sequence silencing by H3K9me3 MtSig contributed to these phenotypes, and inhibiting H3K9me3 MtSig in patient-derived GBM cells suppressed proliferation and increased immune responses. H3K9me3 MtSig serves as an independent prognostic factor and potential therapeutic target.

Chaetocin, an SUV39H1 inhibitor, mimics the effects of SUV39H1 knockdown, reducing GSC stemness and sensitizing cells to temozolomide, a standard GBM chemotherapy...Clinically, high SUV39H1 expression correlates with poor glioma prognosis, supporting its relevance as a therapeutic target. This study identifies SUV39H1 as a crucial regulator of GSC maintenance and a promising therapeutic target to improve GBM treatment and patient outcomes.