miR-20a promotes cell proliferation and migration by targeting DLC1 in nasopharyngeal carcinoma

The role of miR-20a in nasopharyngeal carcinoma (NPC) and its relationship with the tumor suppressor DLC1 remain incompletely understood. We analyzed miR-20a expression in public datasets and clinical samples, assessed cell proliferation and migration, and examined target regulation using a dual-luciferase reporter assay. Tumor growth was evaluated in a subcutaneous xenograft model. miR-20a was elevated in NPC tissues and cell lines, and higher expression was associated with poorer survival in a public dataset. miR-20a overexpression promoted cell proliferation and migration, altered epithelial–mesenchymal transition-associated markers, increased MMP-2, MMP-7 and MMP-9 protein levels, and enhanced xenograft growth. miR-20a inhibition increased DLC1 expression and the activity of a reporter containing the wild-type DLC1 3′ untranslated region, without significantly affecting the corresponding mutant reporter. DLC1 knockdown attenuated the inhibitory effects of miR-20a inhibition on colony formation and migration and counteracted associated protein changes. These findings support DLC1 as a functional mediator of miR-20a-associated malignant phenotypes in NPC and provide a rationale for further preclinical investigation of the miR-20a/DLC1 axis.