Inhibition of RACGAP1 sensitizes triple-negative breast cancer cells to ferroptosis by regulating CPT1A-dependent fatty acid metabolism.

ABSTRACT:

Background

Triple-negative breast cancer (TNBC) is highly aggressive tumor with limited therapeutic options. Studying the molecular mechanisms underlying TNBC is necessary to address the unmet need in novel therapeutic targets. TNBC is demonstrated to have robust fatty acid (FA) metabolism activity, and recent studies proposed the linkage of FA metabolism with ferroptosis sensitivity. Hence, this study aimed to explore the targets that may regulate FA metabolism to sensitize TNBC cells to ferroptosis.

Methods

RNA-sequencing data in The Cancer Genome Atlas (TCGA) and four microarray datasets in Gene Expression Omnibus (GEO) database were analyzed to identify key target RACGAP1, followed by a series of functional experiments to explore the exact role of RACGAP1 in two TNBC cel

SUBMITTER: Zhou Z 

PROVIDER: S-EPMC12729191 | biostudies-literature | 2025 Dec

REPOSITORIES: biostudies-literature