MiR-96-5p is an oncogene in lung adenocarcinoma and facilitates tumor progression through ARHGAP6 downregulation.

Accumulating investigations illustrated that miRNA acts as a key regulator in tumor progression, whereas regulatory role of miR-96-5p in lung adenocarcinoma (LUAD) is warranted. Thus, we sought to probe mechanism of miR-96-5p in this disease. Through bioinformatics analysis, miR-96-5p level in normal tissue and LUAD tissue in TCGA database were obtained. Meanwhile, mRNA expression dataset was analyzed to obtain downregulated mRNAs binding to miR-96-5p. qRT-PCR assessed miR-96-5p and ARHGAP6 mRNA in LUAD. Western blot assessed protein level of ARHGAP6 in LUAD. Dual-luciferase reporter gene detection verified targeting relationship of miR-96-5p and ARHGAP6. Biological functional experiments such as CCK-8, colony formation, scratch healing, and Transwell assessed cell proliferation, migration, and invasion. MiR-96-5p was overexpressed, which fostered LUAD cell proliferation, migration, and invasion. ARHGAP6 was downregulated in LUAD and targeted by miR-96-5p. ARHGAP6 upregulation prominently restored promotion of miR-96-5p on cell progression. MiR-96-5p could stimulate LUAD progression through targeting ARHGAP6. This study generates a novel direction and lays a theoretical basis for targeted therapy.