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The long noncoding RNA LINC01012 is known to play critical roles in tumorigenesis. However, its underlying regulatory mechanisms remain largely unclear in hepatitis B (HBV)-related hepatocellular carcinoma (HCC). This study aimed to identify the potential protein targets of LINC01012 and to elucidate the molecular mechanisms by which LINC01012 promotes HBV-HCC progression. Bioinformatics analysis was employed to investigate whether LINC01012 expression is abnormal in HCC and whether such abnormalities hold clinical significance. HBV-HCC cases were collected to validate LINC01012 expression levels and clinical value in HBV-HCC. The effects of LINC01012 knockdown on cell proliferation, migration, and invasion were studied using HBV-HCC cell lines (HepAD38 and HepG2.2.15). Bioinformatics predictions combined with RIP and RNA pulldown experiments were employed to predict and validate RBPs interacting with LINC01012 and its downstream target genes. The results showed that LINC01012 was significantly upregulated in HBV-HCC tissues and serum and correlated with advanced T stage, TNM stage, vascular invasion, and poor survival. Multivariate Cox analysis confirmed high LINC01012 expression as an independent prognostic factor (HR = 2.52, 95%CI: 1.21-5.24). Functional studies demonstrated that LINC01012 knockdown suppressed proliferation, migration, invasion, and expression of α-SMA. Mechanistically, LINC01012 directly interacted with HNRNPL, which in turn promoted the stability of the oncogenic splice variant SLK-S. Silencing LINC01012 reduced both HNRNPL and SLK-S expression. In conclusion, LINC01012 may act as an oncogenic lncRNA in HBV-HCC by stabilizing SLK-S via interaction with HNRNPL, promoting malignant phenotypes, and predicting poor prognosis. These findings highlight its potential as a therapeutic target and prognostic biomarker in HBV-driven HCC.