Throwing the cancer switch: reciprocal roles of polycomb and trithorax proteins.
The discovery that cancer can be governed above and beyond the level of our DNA presents a new era for designing therapies that reverse the epigenetic state of a tumour cell. Understanding how altered chromatin dynamics leads to malignancy is essential for controlling tumour cells while sparing normal cells. Polycomb and trithorax group proteins are evolutionarily conserved and maintain chromatin in the 'off' or 'on' states, thereby preventing or promoting gene expression, respectively. Recent work highlights the dynamic interplay between these opposing classes of proteins, providing new avenues for understanding how these epigenetic regulators function in tumorigenesis.
Mills
Alea A
AA
Cold Spring Harbor Laboratory, Cold Spring Harbor, New York 11724, USA. mills@cshl.edu
D000818:Animals; D002843:Chromatin / Q000502:physiology; D011495:Histone-Lysine N-Methyltransferase; D006801:Humans; D051788:Myeloid-Lymphoid Leukemia Protein / Q000502:physiology*; D009369:Neoplasms / Q000473:pathology / Q000503:physiopathology*; D063146:Polycomb-Group Proteins; D012097:Repressor Proteins / Q000502:physiology*
D002843:Chromatin; C497422:KMT2A protein, human; D063146:Polycomb-Group Proteins; D012097:Repressor Proteins; D051788:Myeloid-Lymphoid Leukemia Protein; D011495:Histone-Lysine N-Methyltransferase