Abstract
In this study, our findings indicated that FOXO1 expression frequently decreased in glioma tissues and cells. FOXO1 expression decrease correlated with glioma progression and predicted a worse overall survival of glioma patients. Restored FOXO1 expression inhibited glioma cells invasion and suppressed glioma cells proliferation in vitro and growth in vivo. Additionally, we found that KLF4 expression frequently increased in glioma tissues and negatively correlated with FOXO1 expression. Bioinformatics analysis and experimental results indicated that KLF4 transcriptionally repressed FOXO1 expression in glioma cells. Moreover, KLF4 expression increase correlated with glioma progression and predicted a poorer overall survival of glioma patients. KLF4 knockdown attenuated glioma cells invasion and growth. These data provide a rationale for targeted intervention on KLF4-FOXO1 signaling pathway to suppress glioma progression.
Highlights
Malignant glioma, is the most common and type of malignant primary brain tumors in human and is characterized by high morbidity and mortality rates
These results indicated that FOXO1 expression is repressed in gliomas
The tumor suppressive role of FOXO1 has been well characterized for some cancer types, little is known of its biological function and significance in glioma
Summary
Malignant glioma, is the most common and type of malignant primary brain tumors in human and is characterized by high morbidity and mortality rates. Despite the advancements in both diagnostic modalities and therapeutic strategies over the past several decades, the prognosis of malignant glioma still remains poor [2]. This poor prognosis is mainly due to the invasive potential of malignant glioma, which precludes complete resection and enhances resistance to therapy [3]. FOXOs have been widely studied for their broad roles in physiological process, including cell cycle arrest, apoptosis, angiogenesis, stress resistance, energy metabolism, and stem cell differentiation [5]. The precise expression pattern and role of FOXO1 in glioma remain elusive
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