Objective <p>This study aimed to clarify the role of LINC00907 in hepatocellular carcinoma (HCC) and its underlying molecular mechanisms.</p> Methods <p>The research population comprised 117 participants diagnosed with HCC. The expressions of LINC00907 and miR-24-3p in both tissue specimens and cell lines, along with those of EMT markers and the MMP-2 and MMP-9, were measured using RT-qPCR. Cellular proliferation was measured with the CCK-8 assay, while apoptotic rates were determined by flow cytometry. The direct interactions between LINC00907, miR-24-3p, and PDGFRL were validated by dual luciferase reporter and RNA pull-down assays. HCC cells were transfected with constructs specifically modulating LINC00907 and miR-24-3p to investigate the impact of their expression on malignant phenotypic behaviors.</p> Results <p>LINC00907 expression was significantly downregulated in HCC, whereas miR-24-3p expression was upregulated. Low LINC00907 expression was linked to significantly worse overall survival, as determined by Kaplan-Meier analysis. The upregulation of LINC00907 led to the suppression of cell proliferation and EMT, while inducing apoptosis and reducing the levels of MMP-2 and MMP-9. LINC00907 was shown to directly target and negatively regulate miR-24-3p. Furthermore, rescue experiments demonstrated that upregulation of miR-24-3p counteracted the tumor-suppressive effects mediated by LINC00907 overexpression in HCC cells.</p> Conclusion <p>LINC00907 exerts tumor-suppressive effects by targeting and negatively regulating miR-24-3p, thereby influencing proliferation, apoptosis, and EMT in HCC cells.</p> Graphical Abstract <p></p>