Aim: To investigate the effects of SKA3 on cell proliferation and metastasis in non-small-cell lung cancer (NSCLC) and its underlying mechanism. Methods: Immunohistochemistry was employed to analyze the expression of SKA3 in NSCLC. CCK-8 assay, EdU assay, Transwell assay and flow cytometry analysis were employed to assess cell proliferation, metastatic potential and apoptosis in vitro, respectively. A lung metastasis model was used to evaluate metastasis of NSCLC cells in vivo. A luciferase reporter gene assay was conducted to verify the targeting relationship. Results: SKA3 exhibited high expression in NSCLC tissues and cells. Overexpression of SKA3 remarkably accelerated cell proliferation and metastasis and suppressed apoptosis of NSCLC cells and promoted lung metastasis in a mouse model. miR-128-3p repressed SKA3 expression by targeting it. Conclusion:miR-128-3p inhibited the progression of NSCLC through targeting SKA3.
Keywords: NSCLC; SKA3; apoptosis; invasion; lung metastasis; miR-128-3p; migration; proliferation.
It is reported that the protein SKA3 can promote the growth and spread of cancer cells in multiple tumors. However, the biological role and action of SKA3 in the progression of non-small-cell lung cancer remain unknown. This study showed that a high level of SKA3 was linked with poor outcomes in non-small-cell lung cancer patients. SKA3 overexpression facilitated cell growth and spread, but inhibited cell death. miR-128-3p directly targeted SKA3 and reversed its effects. Our work suggests that SKA3 and miR-128-3p are promising therapy targets and diagnostic markers for non-small-cell lung cancer.