Ontology highlight
ABSTRACT: Background
Several mechanisms are involved in the resistance to endocrine therapy (ET) in estrogen receptor (ERα)-positive breast cancer (BC), including acquired mutations of ERα gene (ESR1). For example, the frequent mutation, Y537S, was shown to trigger a constitutively active receptor leading to reduced affinity for both agonist and antagonist ligands. The development of more comprehensive therapies remains a challenge in BC patients exhibiting activating mutations in ERα. Here, we show that Poly (ADP-ribose) polymerase-1 (PARP-1) may be considered as a novel therapeutic target in ERα-positive BC.Methods
ERα wild type or Y537S mutated MCF7 and T47D BC cell lines were used as model systems. Immunoblotting, immunofluorescence, gene silencing, real-time PCR, promoter assays
SUBMITTER: Zicarelli A
PROVIDER: S-EPMC12168341 | biostudies-literature | 2025 Jun
REPOSITORIES: biostudies-literature