AI Article Synopsis
- Histone deacetylases (HDACs) are key players in regulating gene transcription and are linked to various diseases, such as cancer, primarily through transcriptional repression.
- Research indicates that while the SIN3B protein is involved in cell-cycle gene repression, its knockout doesn't broadly activate these genes in certain non-proliferating cell lines.
- Findings reveal that the E2F:RB and DREAM complexes can effectively repress cell-cycle genes independently of HDAC activity, suggesting other mechanisms at play in gene regulation.
Article Abstract
Histone deacetylases (HDACs) play a crucial role in transcriptional regulation and are implicated in various diseases, including cancer. They are involved in histone tail deacetylation and canonically linked to transcriptional repression. Previous studies suggested that HDAC recruitment to cell-cycle gene promoters via the retinoblastoma (RB) protein or the DREAM complex through SIN3B is essential for G1/S and G2/M gene repression during cell-cycle arrest and exit. Here we investigate the interplay among DREAM, RB, SIN3 proteins, and HDACs in the context of cell-cycle gene repression. Knockout of SIN3B does not globally derepress cell-cycle genes in non-proliferating HCT116 and C2C12 cells. Loss of SIN3A/B moderately upregulates several cell-cycle genes in HCT116 cells but does so independently of DREAM/RB. HDAC inhibition does not induce general upregulation of RB/DREAM target genes in arrested transformed or non-transformed cells. Our findings suggest that E2F:RB and DREAM complexes can repress cell-cycle genes without relying on HDAC activity.
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|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11126580 | PMC |
| http://dx.doi.org/10.1038/s41467-024-48724-0 | DOI Listing |
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