Hepatocellular carcinoma (HCC) is a malignant tumor with high morbidity and mortality. Many lncRNAs play important regulatory roles in the pathogenesis of HCC, but the mechanism of action of LINC00342 in the progression of HCC remains unclear. In this study, we assessed 24 pairs of HCC tissues and adjacent normal tissues as well as HCC cells and a nude mouse model of HCC. Gene and protein expression was evaluated by flow cytometry, CCK-8, RIP, colony formation assay, and TUNEL staining. This study revealed that LINC00342 was highly expressed in HCC tissues and cells. LINC00342 knockdown significantly inhibited the proliferation and migration of HCC cells, promoted apoptosis, inhibited tumor growth in vivo, and increased the sensitivity of HCC cells to cisplatin. The opposite effect was observed in LINC00342-overexpressing cells. Mechanistically, ZNF384 and m6A methylation can promote the transcription and stability of LINC00342, and LINC00342 can bind to DAPK1, which inhibits Cyt C release and the activation of caspase family proteins to accelerate HCC progression. Our study indicated that the inhibition of LINC00342 expression may represent a new breakthrough for HCC treatment.