The aim of current study is to explore the epigenetic changes and function of KCTD8 in human hepatocellular carcinoma (HCC). HCC cell lines and tissue samples were employed. Methylation specific PCR, flow cytometry, immunoprecipitation and xenograft mouse models were used. was methylated in 44.83% (104/232) of HCC and its methylation may act as an independent poor prognostic marker. KCTD8 expression was regulated by DNA methylation. KCTD8 suppressed HCC cell growth both and via inhibiting PI3K/AKT pathway. Methylation of is an independent poor prognostic marker, and epigenetic silencing of KCTD8 increases the malignant tendency in HCC.
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http://dx.doi.org/10.1080/17501911.2024.2370590 | DOI Listing |
Cancers (Basel)
December 2024
Hugo W. Moser Research Institute at Kennedy Krieger, Baltimore, MD 21205, USA.
: CSCs are critical drivers of the tumor and stem cell phenotypes of glioblastoma (GBM) cells. Chromatin modifications play a fundamental role in driving a GBM CSC phenotype. The goal of this study is to further our understanding of how stem cell-driving events control changes in chromatin architecture that contribute to the tumor-propagating phenotype of GBM.
View Article and Find Full Text PDFInt J Mol Sci
January 2025
Department of Experimental Medicine, Tor Vergata University of Rome, 00133 Rome, Italy.
MicroRNA (miR)-126 is frequently downregulated in malignancies, including breast cancer (BC). Despite its tumor-suppressive role, the mechanisms underlying miR-126 deregulation in BC remain elusive. Through silencing experiments, we identified Early B Cell Factor 1 (EBF1), ETS Proto-Oncogene 2 (ETS2), and Krüppel-Like Factor 2 (KLF2) as pivotal regulators of miR-126 expression.
View Article and Find Full Text PDFInt J Mol Sci
January 2025
Arthritis and Clinical Immunology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK 73104, USA.
Systemic lupus erythematosus (SLE) is a complex autoimmune disorder characterized by widespread inflammation and autoantibody production. Its development and progression involve genetic, epigenetic, and environmental factors. Although genome-wide association studies (GWAS) have repeatedly identified a susceptibility signal at 16p13, its fine-scale source and its functional and mechanistic role in SLE remain unclear.
View Article and Find Full Text PDFPlants (Basel)
December 2024
Department of Earth and Environmental Sciences, University of Pavia, Via S. Epifanio 14, 27100 Pavia, Italy.
Paramutation, a specific epigenetic phenomenon first identified in by Alexander Brink in the 1950s, has since been observed in different plant and animal species. What sets paramutation apart from other gene silencing processes is its ability for one silenced allele (referred to as paramutagenic) to silence another allele (paramutable) in trans. The resultant silenced allele (paramutated) remains stable across generations, even after separating from the paramutagenic allele, and acquires paramutagenic properties itself.
View Article and Find Full Text PDFNat Commun
January 2025
Infinity, Toulouse Institute for Infectious and Inflammatory Diseases, University of Toulouse, Inserm U1291, CNRS U5051, Toulouse, France.
Protective immune responses require close interactions between conventional (Tconv) and regulatory T cells (Treg). The extracellular mediators and signaling events that regulate the crosstalk between these CD4 T cell subsets have been extensively characterized. However, how Tconv translate Treg-dependent suppressive signals at the chromatin level remains largely unknown.
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