FOXG1, a transcriptional factor belonging to the Forkhead Box (Fox) superfamily, is highly expressed in the brain tissue during brain development and plays an important role in cellular proliferation. Recently, FOXG1 was reported to play important roles in oncogenesis, wherein its abnormal expression regulates tumor cell proliferation. However, the expression and role of FOXG1 in lung cancer remain largely unknown. This study investigated the clinical significance, expression, and role of FOXG1 in lung cancer. We found that FOXG1 was highly expressed in lung cancer tissues. MTT, CCK-8 and colony formation assays showed that FOXG1 overexpression could enhance the proliferation of A549 lung cancer cells. Flow cytometry analysis revealed that FOXG1 promoted the cell cycle and suppressed cell apoptosis. Additionally, the expression levels of PTEN, phosphorylated AKT, mTOR, p53, and Bax were significantly altered in response to changes in FOXG1 expression, indicating that FOXG1 regulated the PI3K pathway. Furthermore, in the xenograft mouse model, the upregulated FOXG1 expression strongly promoted tumor growth. In conclusion, these results suggested that FOXG1 was a critical regulator of the proliferation of lung cancer cells and enhanced tumor growth in vivo.
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