Prominin 2 knockdown inhibits the growth, migration, and invasion of non-small cell lung cancer cells by repressing phosphatidylinositol 3 kinase/protein kinase B pathway.

OBJECTIVE

The prognosis of patients with non-small cell lung cancer (NSCLC) is poor, and this malignancy represents a grievous danger to human health due to its high rates of recurrence and metastasis. Previous studies have linked prominin 2 (PROM2) to certain cancers. However, the impact of PROM2 on the biological behavior of NSCLC cells and regulatory pathways has rarely been explored. Therefore, the study aims to elucidate the roles and regulatory mechanisms of PROM2 in the cell function of NSCLC by interfering with PROM2.

MATERIAL AND METHODS

PROM2 messenger ribonucleic acid (mRNA) and protein expression levels in NSCLC cells were analyzed by applying quantitative real-time polymerase chain reaction and Western blot analysis. Phosphatidylinositol 3 kinase (PI3K), protein kinase B (AKT), and phosphorylated-AKT (p-AKT) protein levels were evaluated through Western blot analysis. Cell counting kit-8 and Transwell assays were used to evaluate NSCLC cell proliferation, migration, and invasion.

RESULTS

PROM2 mRNA protein levels drastically increased in NSCLC tissues and cells. High PROM2 mRNA level was related to the poor prognosis of patients with NSCLC. PROM2 silencing remarkably repressed NCI-H520 and A549 cell proliferation, migration, and invasion. Furthermore, PI3K and p-AKT protein levels clearly decreased after PROM2 silencing. Importantly, rescue experiments elucidated that PI3K/AKT pathway activation could reverse the inhibitory effect of PROM2 silencing on the proliferation, migration, and invasion of NCI-H520 and A549 cells.

CONCLUSION

This study verified that PROM2 knockdown inhibits the growth, migration, and invasion of NSCLC by repressing the PI3K/AKT pathway.