Objective：To investigate the functional impact of lactate on triple - negative breast cancer（TNBC）malignancy and elucidate an m6A-dependent epigenetic mechanism through which insulin-like growth factor 2 mRNA-binding protein 3（IGF2BP3） orchestrates metabolic reprogramming via regulation of EP300. Methods：TNBC cells were treated with exogenous sodium lactate supplementation to investigate their oncogenic effects. Cell proliferation and migration were assessed via CCK -8，colony formation， wound healing，and Transwell assays. Stable IGF2BP3-knockdown cell models were established using shRNA lentiviral vectors，with histone lactylation modification levels analyzed by Western blot. RNA immunoprecipitation sequencing（RIP - seq）and m6A - specific methylated RNA immunoprecipitation sequencing（MeRIP-seq）were used to identify IGF2BP3’s m6A target genes，validated by qRT- PCR and Western blot for key molecule expression. Results：Sodium lactate treatment significantly enhanced TNBC cell proliferation and migration，with pan -lactylation levels increasing dose -dependently. IGF2BP3 knockdown reduced histone lactylation. Integrated RIP - seq/MeRIP - seq analysis identified 699 candidate genes whose transcripts bore both IGF2BP3 - specific binding and m6A modifications，significantly enriched in epigenetic regulation and metabolic pathways. IGF2BP3-binding regions on EP300 transcripts overlapped extensively with m6A sites，and EP300 expression was markedly downregulated post - IGF2BP3 knockdown. Conclusion：Exogenous lactate drives TNBC malignant progression by orchestrating pan - lactylation modifications. IGF2BP3 regulates EP300 expression through m6A - dependent mechanisms，mediating the synergistic interplay between histone lactylation and metabolic reprogramming to drive TNBC progression. These findings provide a theoretical basis for novel therapeutic strategies targeting metabolism-epigenetics crosstalk.