Potential regulatory role of the m 6A-lncRNA axis in breast cancer: molecular mechanisms and therapeutic implications.

Abstract

N6-methyladenosine (m ⁶A) modification, the most prevalent internal modification in eukaryotic messenger RNAs (mRNAs), has emerged as a crucial regulator of various biological processes. This reversible epigenetic modification is dynamically regulated by methyltransferases (writers), demethylases (erasers), and m ⁶A-binding proteins (readers). Aberrant m ⁶A modification is associated with the initiation, progression, and metastasis of breast cancer, highlighting its potential as a therapeutic target. Long non-coding RNAs (lncRNAs), a class of non-protein-coding transcripts longer than 200 nucleotides, are also involved in breast cancer development through diverse mechanisms. Increasing evidence suggests a complex interplay between m ⁶A modifications and lncRNAs in breast cancer, with lncRNAs modulating m ⁶A regulators and m ⁶A-modified lncRNAs exerting functional effects. This review comprehensively summarizes the current understanding of the m ⁶A-lncRNA axis in breast cancer, including the molecular mechanisms underlying its interaction and its effects on breast cancer biological processes, such as proliferation, apoptosis, migration, invasion, and therapy resistance, and highlights the potential of this axis as a diagnostic and therapeutic biomarker. Additionally, we discuss the challenges and future directions in this rapidly evolving field, aiming to provide insights for the development of novel therapeutic strategies for breast cancer.