Lung cancer is the most common
cancer in males and females and ~40% of
lung cancer cases are
adenocarcinomas. Previous studies have demonstrated that myristoylated
alanine rich
protein kinase C substrate (MARCKS) is upregulated in several types of
cancer and is associated with poor prognosis in patients with
breast cancer. However, its expression level and role in
lung adenocarcinoma remain unknown. Therefore, the aim of the present study was to investigate the expression level and biological functions of MARCKS like 1 (MARCKSL1), a member of the MARCKS family, in
lung adenocarcinoma. The expression level of MARCKSL1 was examined in human
lung adenocarcinoma tissues and cell lines. MARCKSL1-specific small interfering RNAs effectively suppressed its expression level and significantly inhibited the proliferation, migration and invasion of
lung adenocarcinoma cells. Additionally, the role of MARCKSLI in the regulation of
metastasis was examined. Silencing MARCKSL1 decreased the expression of the epithelial-mesenchymal transition (EMT)-associated
proteins E-cadherin,
N-cadherin,
vimentin and snail family transcriptional repressor 2, and decreased the phosphorylation level of AKT. The results obtained in the current study suggested that MARCKSL1 promoted the progression of
lung adenocarcinoma by regulating EMT. MARCKSLI may have prognostic value and serve as a novel therapeutic target in
lung adenocarcinoma.