Department of Oncology, Affiliated Cancer Hospital of Zhengzhou University/Henan Cancer Hospital, Zhengzhou, Henan Province, China.
Eur Rev Med Pharmacol Sci. 2021 Jan;25(1):145-153. doi: 10.26355/eurrev_202101_24378.
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.
肺腺癌的发病率在所有恶性肿瘤中位居第一。目前，肺腺癌的诊断方法很多，但成熟或具有理想应用前景的方法却很少。我们旨在探讨 VRK2 在肺腺癌发生发展中的作用及其可能的调节机制。
采用 Western blot 和 qRT-PCR 检测 VRK2 的表达。采用流式细胞术、Western blot 和 Caspase-3 比色法试剂盒评估细胞凋亡水平。通过细胞周期检测、划痕愈合和 Transwell 侵袭实验评估细胞增殖、迁移和侵袭能力。荧光素酶实验验证 VRK2 与 miR-145-5p 的关系。通过裸鼠异种移植模型检测 FGD5-AS1 对脑胶质瘤肿瘤发生的影响。
VRK2 在肿瘤组织和细胞系中明显增加。通过调节 ERK1/2/AKT 信号通路，缺失 VRK2 可促进 A549 细胞的凋亡水平，并抑制其增殖、迁移和侵袭。荧光素酶实验报告 VRK2 可以与 miR-145-5p 结合。miR-145-5p 的水平与 VRK2 的表达呈负相关，并参与 VRK2 调节肿瘤进展。肿瘤生长实验表明，沉默 VRK2 可通过靶向 miR-145-5p 抑制肿瘤的发生，从而抑制 ERK1/2/AKT 通路的激活。
敲低 VRK2 通过靶向 miR-145-5p 调控 ERK1/2/AKT 信号通路，抑制肺腺癌的发展，为肺腺癌的临床治疗提供了一些新的实验依据。
