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RNA modifications constitute an important layer of post-transcriptional gene regulation, yet their collective contribution to breast cancer progression remains poorly understood. While individual epitranscriptomic marks have been implicated in tumorigenesis, how distinct RNA modifications and their regulators converge to shape aggressive cancer phenotypes is largely unexplored. Here, we investigate the coordinated roles ofRNA modification pathways in breast cancer, with a focus on triple-negative breast cancer (TNBC). By analyzing expression patterns of 49 mRNA modification regulators in the SCAN-B breast cancer cohort, we identify subtype-specific epitranscriptomic signatures and reveal coordinated upregulation of multiple RNA modification pathways – including m6A, m5C, pseudouridine, and RNA editing – in TNBC. Several regulators within these pathways are associated with poor patient survival, and co-occurrence of m5C- and pseudouridine-related factors suggests a shared regulatory module linked to enhanced translational activity. We further demonstrate that dynamic m6A regulation contributes to TNBC adaptation under hypoxic stress. Using single-nucleotide–resolution m6A mapping combined with translation and mRNA stability profiling, we show that hypoxia-induced m6A deposition within coding regions is associated with ribosome collision and increased transcript stability, challenging the prevailing view of m6A as a predominantly destabilizing modification. In parallel, we uncover non-canonical functions of the m6A methyltransferase METTL3, showing that cytoplasmic METTL3 promotes vesicle trafficking and invasive behavior independently of its catalytic activity through interaction with the exocyst component EXOC7. Finally, we identify a role for ribosomal RNA 2′-O-methylation in TNBC aggressiveness, demonstrating that fibrillarin-dependent ribosome remodeling selectively regulates oncogenic translation programs. Together, these findings reveal that coordinated RNA modification pathways and non-traditional functions of epitranscriptomic regulators converge to drive translational reprogramming and aggressive behavior in breast cancer.