<p>This study aimed to investigate the role of methyltransferase-like 14 (METTL14) in regulating proliferation and glycolysis in prostate cancer (PCa) through m6A modification of LINC01138. The expression of METTL14 and LINC01138 was analyzed in PCa tissues and cell lines (PC-3 and 22Rv1 cells). Gain- and loss-of-function experiments were performed to evaluate their effects on cell proliferation, migration, invasion, apoptosis, and glycolysis. m6A-related assays were conducted to examine the interaction between METTL14 and LINC01138. In addition, a xenograft mouse model was established to assess the in vivo role of METTL14 in PCa progression. METTL14 was significantly downregulated in prostate cancer and its low expression correlated with advanced TNM stage and distant metastasis. Functional experiments showed that METTL14 overexpression suppressed proliferation, migration, invasion, and glycolytic activity in PCa cells, whereas METTL14 knockdown produced the opposite effects. Mechanistically, METTL14 promoted the m6A modification of LINC01138, leading to its downregulation. Rescue experiments further demonstrated that LINC01138 overexpression reversed the inhibitory effects of METTL14 on tumor progression and glycolysis. In vivo, METTL14 overexpression reduced tumor growth and LINC01138 expression in xenograft models, consistent with the in vitro findings. These findings suggest a potential role of the METTL14-LINC01138 axis in prostate cancer progression and glycolysis. Further studies are warranted to elucidate the precise downstream mechanisms linking LINC01138 to glycolysis and malignant behavior. </p>