N6-methyladenosine (m6A) modification is the most common epitranscriptomic modification in eukaryotic RNA and has garnered extensive attention in the context of breast cancer research. The m6A modification significantly impacts tumorigenesis and tumor progression by regulating RNA stability, splicing, translation, and degradation. In this review we summarize recent advances in understanding the roles of m6A modification in the mechanisms underlying angiogenesis and vasculogenic mimicry in breast cancer. We review how m6A modification and associated transcripts influence relevant factors by affecting key factors and signaling pathways, highlighting the interactions among m6A "writers," "erasers," and "readers," and their overall impact on tumor angiogenesis and vasculogenic mimicry, as well as potential new therapeutic targets.
Keywords: Angiogenesis; Breast cancer; Therapeutic implications; Vasculogenic mimicry; m(6)A modification.
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