microrna-642a-5p targets dna damage-inducible transcript 4 to suppress hepatitis b virus hepatoma carcinoma cell

Background: hepatocellular carcinoma (hcc) is one of the most prevalent malignant tumors in clinical practice, with hepatitis b virus (hbv) being the most common risk factor for hcc. micrornas (mirnas) have emerged as a new marker for disease diagnosis and molecularly targeted therapies; however, the mechanism of mir-642a-5p in hbv-associated hcc remains unclear. objectives: the aim of this study was to investigate the expression of mir-642a-5p, which targets dna damage-inducible transcript 4 (ddit4), in hbv-associated hcc, and its effect on the proliferation, migration, and invasion of hbv-positive hcc cells. methods: mir-642a-5p in the serum of patients with hbv-associated liver cancer (lc), as well as mir-642a-5p and ddit4 mrna in lc tissues and cells, and hbv dna in hbv-positive cells were detected. the targeting of ddit4 by mir-642a-5p and the progression of cells were also examined. all cell experiments were repeated five times. results: the results indicated that levels of mir-642a-5p were decreased, while levels of ddit4 were increased in the serum, tissues, and cells of hbv-positive hcc patients. overexpression of mir-642a-5p inhibited the progression of hbv-positive hcc cells, suppressed hbv dna replication, cell proliferation, and invasion, and promoted apoptosis in hepg2.2.15 cells. conclusions: in addition, mir-642a-5p directly targeted ddit4, and knockdown of ddit4 reversed the effects of mir-642a-5p upregulation, promoting the progression of hbv-positive hcc cells. in conclusion, mir-642a-5p is expressed at low levels in hbv-associated hcc and inhibits hbv dna replication and tumor progression in hbv-positive hcc by targeting ddit4. this study provides a foundation for molecular targeted therapy in hbv-positive hcc.