Wolf-Hirschhorn syndrome candidate gene 1 (WHSC1), a histone methyltransferase, has been implicated in various tumor development processes by regulating target gene expression. However, the role of WHSC1 in glioblastoma remains unexplored. This study investigates the impact of WHSC1 in glioblastoma and its association with prognosis. Our findings reveal that WHSC1 is overexpressed in glioblastoma and correlates with poor patient outcomes. Functional assays demonstrate that the reduction of WHSC1 significantly impairs cell proliferation and tumorigenicity. Mechanistically, WHSC1 modulates PLK1 expression by binding to its promoter region, leading to the activation of the PLK1-AKT pathway, and regulating H3K36 dimethylation levels. Furthermore, YBX1 can cooperate with WHSC1 to activate PLK1 transcription. These results shed light on the potential significance of WHSC1 in glioblastoma and offer a promising avenue for future therapeutic approaches targeting this molecule in glioblastoma treatment.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1016/j.cellsig.2024.111471 | DOI Listing |
Cell Signal
December 2024
The First Affiliated Hospital of Ningbo University, Ningbo 315020, China. Electronic address:
Exp Mol Med
June 2019
Department of Life Science, University of Seoul, Seoul, 02504, Korea.
Recent studies on mutations in cancer genomes have distinguished driver mutations from passenger mutations, which occur as byproducts of cancer development. The cancer genome atlas (TCGA) project identified 299 genes and 24 pathways/biological processes that drive tumor progression (Cell 173: 371-385 e318, 2018). Of the 299 driver genes, 12 genes are involved in histones, histone methylation, and demethylation (Table 1).
View Article and Find Full Text PDFNeuro Oncol
February 2008
Surgical Neurology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892-1414, USA.
Dynamic changes in the expression of multiple genes appear to be common features that distinguish transformed cells from their normal counterparts. We compared the proteomic profiles of four glioblastoma multiforme (GBM) tissue samples and four normal brain cortex samples to examine the molecular basis of gliomagenesis. Trypsin-digested protein samples were separated by capillary isoelectric focusing with nano-reversed-phase liquid chromatography and were profiled by mass spectrometric sequencing.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!