〔Abstract〕 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 consisten- cy 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 and 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 .