Hp1bp3 loss links chromatin reorganization to metabolic vulnerability in glioma - PubMed
4 hours ago
- #glioma growth
- #chromatin reorganization
- #methionine metabolism
- High-grade gliomas (HGGs) are aggressive brain tumors with poor prognosis, influenced by metabolic and epigenetic changes.
- Methionine metabolism supports HGG growth by providing S-adenosylmethionine for methylation reactions.
- Dietary methionine restriction in a mouse model reduced tumor proliferation, extended survival, and induced partial nuclear inversion.
- Hp1bp3 was identified as a key regulator interacting with nuclear tethering proteins to mediate chromatin reorganization.
- Loss of Hp1bp3 upregulates histone demethylases, leading to depletion of H3K9me3-marked heterochromatin and accelerated glioma growth.
- Combining methionine restriction with Hp1bp3 loss increased partial nuclear inversion and further suppressed tumor progression.
- Hp1bp3 links methionine metabolism to heterochromatin stability, suggesting dietary methionine modulation can influence chromatin structure to slow tumor growth in HGG.