Objective To investigate the mechanistic role of LncRNA MITA1 in the progression of hepatocellular carcinoma (HCC). Methods qRT-PCR was employed to assess the expression levels of MITA1 mRNA in HCC tissues and cells. The pcDNA3.1 recombinant plasmid vector was utilized to overexpress MITA1. After treatment, SMMC7721 cells were categorized into three groups, the normal group, the OE-MITA1-NC (negative control) group, and the OE-MITA1 (overexpression) group. Cell proliferation was evaluated using a colony formation assay, while cell invasion was assessed via the Transwell assay. Cell viability was determined using the Cell Counting Kit-8 (CCK-8) assay. Protein expression levels of Vimentin, MMP-2, and N-Cadherin were measured by western blotting. Additionally, the dual-luciferase reporter assay was conducted to verify the targeting relationship between MITA1 and miR-30b-3p. Results Compared with adjacent normal liver tissues, HCC tissues and cells exhibited significantly higher expression levels of MITA1 mRNA and lower expression levels of miR-30b-3p mRNA (P<0.05). Under MITA1 overexpression conditions, the OE-MITA1 group demonstrated elevated MITA1 mRNA expression levels (P<0.05). Compared with the normal and OE-MITA1-NC groups, the OE-MITA1 group exhibited increased cell proliferation, invasion capacity, and enhanced cell viability (P<0.05). Furthermore, protein expression levels of Vimentin, MMP-2, and N-Cadherin were significantly higher in the OE-MITA1 group compared with the other two groups (P<0.05). The dual-luciferase reporter assay confirmed a targeting relationship between MITA1 and miR-30b-3p, with MITA1 expression negatively regulating miR-30b-3p expression. Conclusion LncRNA MITA1 can promotes the proliferation, invasion and cell activity of liver cancer by binding miR-30b-3p, MITA1 may serve as a potential therapeutic target for the diagnosis and treatment of HCC.