Centromere protein K (CENPK) plays a key role in regulating the assembly and function of centromeres, which in turn can affect the occurrence and development of various tumors. However, little is known about the biological function of CENPK in lung adenocarcinoma (LUAD).

Material and methods:
We evaluated the relationship between CENPK expression and the clinicopathological characteristics of LUAD patients via a bioinformatics method based on data taken from the TCGA database. Then, the role of CENPK in LUAD was investigated in vitro by using the human LUAD cell line A549. Cell Counting Kit-8 and colony formation assays were used detect the cell proliferation ability. Wound healing and transwell assays were used to detect the cell migration and invasion ability. Epithelial-mesenchymal transition (EMT) markers (E-cadherin, N-cadherin, Snail and vimentin) were measured by western blotting. In addition, a xenograft experiment was used to explore the function of CENPK in vivo.

CENPK is highly expressed in LUAD tissues and cell lines. Moreover, high expression of CENPK in LUAD is significantly associated with stage, lymph node involvement and poor survival. CENPK knockdown significantly decreases the proliferation, migration and invasion ability of A549 cells by EMT both in vitro and in vivo.

CENPK is highly expressed in LUAD and leads to a poor prognosis. CENPK knockdown can suppress the proliferation, migration, and invasion of lung cancer cells via EMT, which may be a valid target for treatment.