5'-Methylthioadenosine Metabolic Reprogramming Drives H3K79 Monomethylation-Mediated PAK2 Upregulation to Promote Cadmium-Induced Breast Cancer Progression by Impairing Autophagic Flux.

ABSTRACT: Cadmium (Cd) is a heavy metal that exhibits strong carcinogenic properties and promotes breast cancer (BC) progression. Autophagic flux dysfunction is involved in Cd-induced BC progression, but the underlying molecular mechanisms remain unclear. Here, it is observed that impaired autophagic flux and metabolic reprogramming are notable features related to Cd-induced proliferation, migration, and invasion in BC cell lines, including T-47D and MCF-7 cells. Through the integration of metabolomics, proteomics, and ingenuity pathway analysis, a metabolite-protein regulatory network is constructed, which revealed that 5'-methylthioadenosine (MTA)-mediated metabolic reprogramming plays a core regulatory role in the epigenetic‒autophagy axis involved in Cd-induced autophagic flux impairment and BC

SUBMITTER: Li J 

PROVIDER: S-EPMC12667465 | biostudies-literature | 2025 Nov

REPOSITORIES: biostudies-literature