The role of long noncoding RNA myocardial infarction-associated transcript in hepatocellular carcinoma: Targeting miR-361-3p to regulate cell proliferation, invasion, and apoptosis

This study aims to investigate the effects of long noncoding RNA myocardial infarction-associated transcript (lncRNA MIAT) targeting miR-361-3p on the proliferation, invasion, and apoptosis of hepatocellular carcinoma (HCC) cells. The expression levels of lncRNA MIAT and miR-361-3p were examined in both cancerous and adjacent non-tumorous tissues of HCC patients. Additionally, their expression was analyzed in THLE-2 and MHCC97L cells. MHCC97L cells were transfected to observe changes in relevant mRNA expression and alterations in cell proliferation, invasion, and apoptosis. Compared with adjacent non-tumorous tissues, cancerous tissues exhibited increased levels of lncRNA MIAT mRNA and decreased levels of miR-361-3p (P < .05). Elevated transcription levels of lncRNA MIAT were more prevalent in patients with lymph node metastasis and advanced TNM staging (P < .05). In MHCC97L cells, compared with THLE-2 cells, there was an increase in lncRNA MIAT mRNA and a decrease in miR-361-3p (P < .05). LncRNA MIAT and miR-361-3p were found to have potential binding sites and exhibit target regulation. Cells in the miR-NC group showed no significant changes in all indicators compared with the negative control group (P > .05). Conversely, cells with low expression of lncRNA MIAT and cyclin D1 mRNA and decreased cell proliferation and invasion numbers showed increased expression of miR-361-3p and phosphatase and tensin homolog mRNA and higher apoptosis rates (P < .05). The group with elevated expression levels demonstrated contrasting patterns (P < .05). LncRNA MIAT is upregulated in HCC tissues. Silencing lncRNA MIAT can elevate miR-361-3p levels, inhibiting the proliferation and invasion of MHCC97L cell structures and promoting apoptosis.