Objectives: Long non-coding RNAs (lncRNA) fulfill vital functions in glioma (GL) advancement. This work attempted to study the role and mechanism of LINC01578 in glioma. Methods: Cancerous and adjacent tissues were collected in pairs from 20 glioma patients who visited The 900th Hospital of Joint Logistic Support Force between February 2021 and June 2022. LINC01578 expression was quantified using Quantitative real-time Polymerase Chain Reaction (qRT-PCR). Additionally, GL U251 and U87 cells and human astrocytes SVGP12 were purchased to validate the expression profiling of LINC01578. Then, LINC01578 short hairpin RNA (sh-LINC01578), LINC01578 overexpression plasmid (oe-LINC01578), empty carrier for sh-LINC01578 (sh-NC) and empty carrier for oe-LINC01578 (oe-NC) were transfected into U251 and U87 cells, respectively. The untreated U251 and U87 cells were set as controls. Cell counting kit-8 (CCK-8), cell cloning, Transwell (R), and cell scratch assays were employed to determine the impacts of LINC01578 on GL cell biological behavior, and Western blotting was adopted to measure apoptosis-related proteins proliferating cell nuclear antigen (PCNA), cleaved Caspase-3 (cl-Caspase-3) and epithelial-mesenchymal transition (EMT) marker proteins E-cadherin, Results: LINC01578 presented a notably higher expression in GL tissues and cells than in adjacent counterparts and SVGP12 (p < 0.05). Enhanced capacities to proliferate, invade and migrate of U251 and U87 cells were observed following oe-LINC01578 transfection, accompanied by elevated PCNA and reduced cl-Caspase-3 levels at the protein level (p < 0.05); While sh-LINC01578 transfection led to weakened U251 and U87 viability and increased cl-Caspase-3 protein expression (p < 0.05). According to the quantification results of EMT marker proteins, oe-LINC01578 transfection promoted EMT in GL cells, while sh-LINC01578 transfection could not (p < 0.05). Conclusions: LINC01578 is kept at high levels in GL and can enhance EMT and the ability of GL cells to proliferate, invade, and migrate, thus participating in the development of GL.