Blocking VRK2 suppresses pulmonary adenocarcinoma progression via ERK1/2/AKT signal pathway by targeting miR-145-5p

The incidence of pulmonary adenocarcinoma locates first in all the malignant tumors in the world. At present, there are many diagnostic methods for pulmonary adenocarcinoma, but there are a few methods that are mature or have ideal application prospects. We aim to explore the role of VRK2 in the occurrence and development of pulmonary adenocarcinoma and its possible regulatory mechanism.

Western blot and qRT-PCR were performed to assess the expression of VRK2. Flow cytometry, Western blot, and Caspase-3 colorimetric assay Kit were used to evaluate the apoptosis level. The proliferation, migration, and invasion ability were measured via cell cycle assay, wound healing, and transwell invasion assay. Luciferase assay verified the relationship between VRK2 and miR-145-5p. The effect of FGD5-AS1 on tumorigenesis of glioma was detected by the xenograft nude mice model.

VRK2 was significantly increased in tumor tissues and cell lines. Loss of VRK2 promoted apoptosis level and inhibited the proliferation, migration, and invasion in A549 cells via regulating the ERK1/2/AKT signal pathway. Luciferase assay reported that VRK2 could bind with miR-145-5p. The level of miR-145-5p was negatively correlated with the expression of VRK2 and involved in VRK2 regulating tumor progression. The tumor growth assay showed that the silencing of VRK2 inhibited tumorigenesis with the inactivating ERK1/2/AKT pathway.

Knockdown of VRK2 inhibited the development of pulmonary adenocarcinoma via regulating the ERK1/2/AKT signal pathway by targeting miR-145-5p, which providing some novel experimental basis for clinical treatment of pulmonary adenocarcinoma.