H3K27

[Cell Death & Disease] Investigators identified PCGF1 as a crucial epigenetic regulator that sustained the stem cell-like phenotype of colorectal cancer (CRC). PCGF1 knockdown inhibited CRC stem cell proliferation and CRC stem cell enrichment.

[Scientific Reports] Investigators found that the histone acetyltransferases inhibitor C646 augmented anti-tumor effects in vitro by inhibiting cell proliferation and cell cycle progression concomitantly with suppression of acetylated H3K9 and H3K27 expression.

[Cell Death & Disease] RNA-sequencing analysis showed a comprehensive downregulation of β cell and α cell identity genes in A-485-treated islets, without upregulation of dedifferentiation markers and derepression of disallowed genes.

[Cancer Cell] Using isogenic Ewing cells, researchers showed STAG2 loss of function profoundly changed the transcriptome but it did not significantly impact EWSR1-FLI1, CTCF/cohesin, or acetylated H3K27 DNA binding patterns.

[Science Translational Medicine] The authors demonstrated that selective HDAC8 inhibition elicited effective and durable responses to immune-checkpoint blockade by co-opting adaptive immunity through enhancer reprogramming.

[Proceedings of the National Academy of Sciences of the United States of America] Researchers specifically depleted H3K36me2 or H3K36me3 in mesenchymal cells, using CRISPR-Cas9 to separately knock out the corresponding methyltransferases NSD1/2 or SETD2.