〔Abstract〕 Objective To investigate the regulatory relationship between long non-coding RNA LINC01578 and c-Myc, and to explore the effect of LINC01578 on the metabolic process of oral squamous cell carcinoma(OSCC). Methods After c-Myc was knocked down in OSCC cell line CAL27, LINC01578, a long non-coding RNA that is positively regulated by c-Myc, was identified by high-throughput sequencing technology. qRT-PCR was employed to measure the expression levels of c-Myc and LINC01578 in OSCC tissues and adjacent normal tissues. Following overexpression or knockdown of c-Myc in CAL27 and HN6 cells, qRT-PCR was conducted to validate the consistency with sequencing results. The binding of c-Myc to the LINC01578 promoter was confirmed using a dual luciferase reporter assay. Seahorse, ATP production and lactate production assays were utilized to examine the impact of c-Myc on glucose metabolism in OSCC via LINC01578. Colony formation assays assessed the proliferative capacity of OSCC cell lines. Results qRT-PCR analysis revealed significantly higher expression levels of c-Myc LINC01578 in OSCC tissues compared to adjacent tissues( P < 0. 05 ) , confirming that c⁃Myc positively regulates LINC01578 expression. Consistent with sequencing data , c⁃Myc overexpression markedly upregulated LINC01578 (P < 0. 001) , while c⁃Myc knockdown led to a significant decrease in LINC01578 levels(P < 0. 000 1) . Dual lu ciferase reporter gene assays demonstrated that c⁃Myc directly targets and transcriptionally enhanced LINC01578 ex⁃ pression(P < 0. 001) . Seahorse experiments indicated that c⁃Myc promoted glucose metabolism in OSCC through LINC01578 regulation(P < 0. 05) . Colony formation assays showed that LINC01578 overexpression enhanced OS⁃ CC cell proliferation , whereas LINC01578 knockdown inhibited it. Conclusion c⁃Myc upregulates LINC01578 expression in OSCC cells , thereby modulating glycolysis and promoting cell proliferation.