PTEN loss promotes oncogenic function of STMN1 via PI3K/AKT pathway in lung cancer

Abstract

Abstract Among all cancer types, lung cancer has already become the leading cause of cancer-related death around the world. The molecular mechanism understanding this development is still needed to be improved to treat lung cancer. Stathmin (STMN1) was initially identified as a cytoplasmic protein phosphorylated responding to cell signal and controlled cell physiological processes. The dysregulation of STMN1 is found in various kinds of tumors. However, the molecular mechanism of STMN1 regulating lung cancer is still unclear. Here, we found that STMN1 was overexpressed in lung cancer tissues and associated with worse survival rates of lung cancer patients. Inhibition of STMN1 suppressed lung cancer cell growth, migration and invasion, and promoted drug sensitivity. Moreover, PTEN loss promoted STMN1 expression via PI3K/AKT pathway. PTEN loss ameliorated the inhibition of cell growth, migration and invasion, and drug sensitivity induced by STMN1 knockdown in lung cancer. The high expression of STMN1 was negatively correlated with the low expression of PTEN in lung cancer specimens. Overall, our work demonstrated that PTEN regulated the oncogenic function of STMN1 in lung cancer.