ACSL3 regulates breast cancer progression via lipid metabolism reprogramming and the YES1/YAP axis.

ABSTRACT:

Objective

Mitochondrial fatty acid oxidation is a metabolic pathway whose dysregulation is recognized as a critical factor in various cancers, because it sustains cancer cell survival, proliferation, and metastasis. The acyl-CoA synthetase long-chain (ACSL) family is known to activate long-chain fatty acids, yet the specific role of ACSL3 in breast cancer has not been determined.

Methods

We assessed the prognostic value of ACSL3 in breast cancer by using data from tumor samples. Gain-of-function and loss-of-function assays were also conducted to determine the roles and downstream regulatory mechanisms of ACSL3 in vitro and in vivo.

Results

ACSL3 expression was notably downregulated in breast cancer tissues compared with normal tissues, and this phenotype

SUBMITTER: Tan S 

PROVIDER: S-EPMC11271223 | biostudies-literature | 2024 Jul

REPOSITORIES: biostudies-literature