Abstract
BACKGROUND MiR-10b can promote the growth of lung cancer cells. LATS2 is reported to regulate lung cancer cell proliferation. We aimed to study the relationship between miR-10b and LATS2 in lung cancer. MATERIAL AND METHODS MiR-10b and LATS2 in lung cancer tissues and cells were measured via real-time polymerase chain reaction (RT-PCR) and western blotting. Luciferase reporter assay and mimic transfection were performed to study relation between miR-10b and LATS2. MiR-10b inhibitor was transfected to downregulate miR-10b expression and LATS2 was further downregulated. Then, the proliferation, apoptosis, migration, and invasion capacity of lung cancer cells were measured, respectively. Lung cancer cells stably transfected with LATS2 and TAZ plasmids were constructed as usual, and the effect of LATS2 overexpression on epithelial-mesenchymal transition (EMT) was determined. RESULTS MiR-10b was upregulated and LATS2 was significantly downregulated in lung cancer. Inhibition of miR-10b restrained the growth of lung cancer cells and accelerated the apoptosis of lung cancer cells. LATS2 is directly bound by miR-10b and silence of LATS2 reversed its inhibitory and promotive effects. Overexpression of LATS2 inhibited the EMT of lung cancer cells by inhibiting the TAZ pathway. CONCLUSIONS MiR-10b was upregulated in lung cancer. Inhibition of miR-10b could restrain the development of lung cancer by increasing LATS2 expression via TAZ.