Ontology highlight
ABSTRACT: Background
Frequent truncation mutations of the histone lysine N-methyltransferase KMT2C have been detected by whole exome sequencing studies in various cancers, including malignancies of the prostate. However, the biological consequences of these alterations in prostate cancer have not yet been elucidated.Methods
To investigate the functional effects of these mutations, we deleted the C-terminal catalytic core motif of Kmt2c specifically in mouse prostate epithelium. We analysed the effect of Kmt2c SET domain deletion in a Pten-deficient PCa mouse model in vivo and of truncation mutations of KMT2C in a large number of prostate cancer patients.Results
We show here for the first time that impaired KMT2C methyltransferase activity drives proliferation and PIN formatio
SUBMITTER: Limberger T
PROVIDER: S-EPMC8966196 | biostudies-literature | 2022 Mar
REPOSITORIES: biostudies-literature