Background
Identification of functional genes or biomarkers may be helpful for developing new treatment strategies in lung adenocarcinoma (LUAD). The centromere protein K (CENPK) gene has been discovered to be overexpressed and could influence tumor progression in several tumor types. However, its role in LUAD has never been revealed. Objectives: The
Conclusions
CENPK was upregulated in LUAD tissues and cells, and the enhancement of CENPK promoted the viability, migration, invasion, and EMT of LUAD cells.
Material and methods
Data from The Cancer Genome Atlas (TCGA) and Oncomine databases was used to analyze the expression of CENPK. The relationship between CENPK expression and the prognosis of LUAD was investigated using Kaplan-Meier and Cox regression analyses. The cell viability was monitored with Cell Counting Kit-8 (CCK-8) and colony forming assays, while migration and invasion were analyzed with a transwell assay. The effect of CENPK on the expression of epithelial-mesenchymal transition (EMT) markers were estimated using western blotting.
Methods
Data from The Cancer Genome Atlas (TCGA) and Oncomine databases was used to analyze the expression of CENPK. The relationship between CENPK expression and the prognosis of LUAD was investigated using Kaplan-Meier and Cox regression analyses. The cell viability was monitored with Cell Counting Kit-8 (CCK-8) and colony forming assays, while migration and invasion were analyzed with a transwell assay. The effect of CENPK on the expression of epithelial-mesenchymal transition (EMT) markers were estimated using western blotting.
Results
CENPK was significantly overexpressed in LUAD tissues and cells (p < 0.01). The overall survival rate in the low CENPK expression group was significantly higher than in the high CENPK expression group (p = 0.003). Furthermore, the overexpression of CENPK facilitated cell viability, migration and invasion of tumor cells, while knockdown of CENPK prevented these behaviors (p < 0.01). Moreover, upregulation of CENPK decreased the expression of E-cadherin and enhanced the expression of N-cadherin, vimentin and Snail in LUAD cells (p < 0.01). Conversely, knockdown of CENPK resulted in the opposite trend (p < 0.01). Conclusions: CENPK was upregulated in LUAD tissues and cells, and the enhancement of CENPK promoted the viability, migration, invasion, and EMT of LUAD cells.