PPARγ acetylation governs mammary adenocarcinoma tumor growth via acetylated residues that determine DNA sequence-specific binding.

ABSTRACT: Peroxisome proliferator-activated receptor γ (PPARγ), which is expressed in a variety of malignancies, governs biological functions through transcriptional programs. Defining the molecular mechanisms governing the selection of canonical versus non-canonical PPARγ binding sequences may provide the opportunity to design regulators with distinct functions and side effects. Acetylation at K268/293 in mouse Pparγ2 participates in the regulation of adipose tissue differentiation, and the conserved lysine residues (K154/155) in mouse Pparγ1 governs lipogenesis in breast cancer cells. Herein, the PPARγ1 acetylated residues K154/155 were shown to be essential for oncogenic ErbB2 driven breast cancer growth and mammary tumor stem cell expansion in vivo. The induction of transcriptional modules gover

SUBMITTER: Tian L 

PROVIDER: S-EPMC12414806 | biostudies-literature | 2025 Sep

REPOSITORIES: biostudies-literature