Table 2_LncRNA AP003469.2 promotes hepatocellular carcinoma progression by regulating cuproptosis via the miR-4732-3p/LIPT1 axis.docx

Subsequent in vitro and in vivo studies confirmed AP003469.2’s biological role in HCC. To understand the fundamental mechanisms, we determined the subcellular localization of the proteins using nuclear–cytoplasmic fractionation and fluorescence in situ hybridization (FISH). The regulatory relationships between miR-4732-3p and LIPT1 and between AP003469.2 and miR-4732-3p were then verified using dual-luciferase reporter assays.

In addition, we utilized Western blotting, copper assays, CCK-8, and immunohistochemistry to evaluate related proteins and markers indicative of cuproptosis.</p>Results<p>A poor prognosis was observed to be positively correlated with elevated expression of AP003469.2 in HCC. In both in vivo and in vitro experimental methods, AP003469.2 stimulated important malignant characteristics in HCC cells, including invasion, migration, and proliferation.

Furthermore, by controlling LIPT1 expression and modulating copper homeostasis and important proteins, including FDX1, SLC31A1, and HSP70, AP003469.2 acts as a molecular sponge for miR-4732-3p, attenuating cuproptosis.</p>Conclusion<p>Our research demonstrated that the AP003469.2/miR-4732-3p/LIPT1 axis could suppress cuproptosis to promote HCC progression. Therefore, AP003469.2 may serve as a target for HCC treatment or diagnosis.</p>