Non-enzymatic SETD1A activity drives breast cancer cell proliferation via cyclin K.

ABSTRACT:

Background

Breast cancer is the most common cancer in women worldwide. SETD1A, a histone H3 lysine-4 methyltransferase, is associated with poor prognosis in breast cancer. While both its enzymatic and non-enzymatic functions are implicated in cancer progression, the specific role of SETD1A in breast cancer remains unclear. This study aimed to elucidate the molecular mechanisms underlying SETD1A dependency in breast cancer.

Methods

SETD1A-high breast cancer cell lines were identified using TCGA and DepMap databases, along with SETD1A knockdown experiments. A CRISPR knockout of SETD1A was performed in a doxycycline-inducible Cas9-expressing KPL-1 breast cancer cell line. RNA-seq, ChIP-seq, CRISPR-tiling screening, and rescue experiments with exogenous SETD1A mutants were perfo

SUBMITTER: Hayashi K 

PROVIDER: S-EPMC12337470 | biostudies-literature | 2025 Aug

REPOSITORIES: biostudies-literature