FOXG1 regulates the proliferation and apoptosis of human lung cancer cells

生物 癌变 细胞生长 PI3K/AKT/mTOR通路 肺癌 癌症研究 细胞凋亡 蛋白激酶B 细胞周期 流式细胞术 癌症 下调和上调 PTEN公司 分子生物学 内科学 医学 基因 遗传学
作者
Yan Chang,Yuqing Wang,Caiting Yang,Xiaoting Zhang,Yongxin Liu,Pan Gong,Huijie Jiang,Yun Pan,Zhenjin Li,Mason Lai
出处
期刊:Heliyon [Elsevier]
卷期号:9 (9): e19540-e19540
标识
DOI:10.1016/j.heliyon.2023.e19540
摘要

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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