ONCOLOGY / RESEARCH PAPER
 
KEYWORDS
TOPICS
ABSTRACT
Introduction:
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 analyzed the relationship between CENPK expression and the clinicopathological characteristics of LUAD patients via bioinformatics methods. Then, the role of CENPK in LUAD was investigated in vitro by using the human LUAD cell line A549.The cell counting kit-8 and colony formation assays were used detect the cell proliferation ability. The wound healing and transwell assays were used to detect the cell migration and invasion ability. The epithelial-mesenchymal transition (EMT) markers (E-cadherin, N-cadherin, Snail and Vimentin) were measured by western blotting.

Results:
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 regulating epithelial-mesenchymal transition (EMT).

Conclusions:
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.

eISSN:1896-9151
ISSN:1734-1922