<p>Long non-coding RNAs (lncRNAs) are instrumental in the progression and regulation of gastric cancer (GC), affecting various cellular processes including gene expression, apoptosis, cell proliferation, and metastasis. N6-methyladenosine (m6A), a dynamic and reversible RNA modification, profoundly influences GC by modulating RNA metabolism and function, impacting RNA stability, maturation, and interactions. The crosstalk between non-coding RNAs (ncRNAs) and m6A modification is pivotal for the stability, maturation, and functional interactions of ncRNAs. Moreover, m6A-modified ncRNAs are integral in GC by regulating vital pathways involved in tumor growth and metastasis. This interaction is critical for the rapid response of cancer cells to environmental changes, facilitating their adaptation and survival. The differential expression of m6A-modified ncRNAs in GC tissues compared to normal tissues can serve as diagnostic and prognostic biomarkers, aiding in patient stratification and personalized treatment plans. Targeting m6A modification emerges as a promising therapeutic strategy for GC. Inhibiting m6A “writers” such as METTL3 can diminish the stability of oncogenic ncRNAs, thereby hindering tumor growth and metastasis. Conversely, augmenting m6A modification on tumor-suppressive ncRNAs can enhance their stability and therapeutic efficacy. This review highlights the key roles of m6A modification and ncRNAs in GC, providing valuable insights for future research and potential clinical applications.</p>