Emerging roles of H3K9me3, SETDB1 and SETDB2 in therapy-induced cellular reprogramming.

ABSTRACT:

Background

A multitude of recent studies has observed common epigenetic changes develop in tumour cells of multiple lineages following exposure to stresses such as hypoxia, chemotherapeutics, immunotherapy or targeted therapies. A significant increase in the transcriptionally repressive mark trimethylated H3K9 (H3K9me3) is becoming associated with treatment-resistant phenotypes suggesting upstream mechanisms may be a good target for therapy. We have reported that the increase in H3K9me3 is derived from the methyltransferases SETDB1 and SETDB2 following treatment in melanoma, lung, breast and colorectal cancer cell lines, as well as melanoma patient data. Other groups have observed a number of characteristics such as epigenetic remodelling, increased interferon signalling, cell cycl

SUBMITTER: Torrano J 

PROVIDER: S-EPMC6408861 | biostudies-literature | 2019 Mar

REPOSITORIES: biostudies-literature