Original Article
Apollon overexpression promotes cell motility of gliomas, and predicts patients’ poor prognosis
Abstract
Background: Apollon has been reported to play an oncogenic role in various human cancers. Glioma cell line SNB-78 has been reported to express an increased level of apollon and had distinct resistance against several anti-cancer drugs. Here, we aimed to investigate the clinical impact of apollon dysregulation in patients with gliomas, and its functions in malignant phenotypes of glioma cells.
Methods: Apollon expression in human gliomas tissues was examined by immunohistochemistry. Associations between apollon expression and various clinicopathological factors as well as patients’ prognosis were then evaluated. Followed by the transfection of an apollon-specific small interfering RNA in glioma cells, cell migration and invasion were measured by transwell assays in vitro.
Results: Immunostainings of apollon protein were mainly shown in tumor cell cytoplasm of glioma tissues, but weakly or negatively observed in nonneoplastic brain tissues. Statistically, the immunoreactive score (IRS) of apollon protein in glioma tissues was significantly higher than that in the corresponding nonneoplastic brain tissues (P=0.013). Additionally, patients with higher IRS often had advanced World Health Organization (WHO) grade (P=0.001) and shorter overall survival time (P=0.01). Further multivariate analysis identified apollon expression as an independent prognostic factor of glioma patients (P=0.03). Functionally, in vitro experiments revealed that loss of apollon could efficiently suppress migration and invasion of glioma cells.
Conclusions: These findings imply that the dysregulation of apollon may be implicated into tumorigenesis and various pathological changes of human gliomas. Importantly, this protein might be a potential prognostic marker and novel therapeutic target for patients with this tumor.
Methods: Apollon expression in human gliomas tissues was examined by immunohistochemistry. Associations between apollon expression and various clinicopathological factors as well as patients’ prognosis were then evaluated. Followed by the transfection of an apollon-specific small interfering RNA in glioma cells, cell migration and invasion were measured by transwell assays in vitro.
Results: Immunostainings of apollon protein were mainly shown in tumor cell cytoplasm of glioma tissues, but weakly or negatively observed in nonneoplastic brain tissues. Statistically, the immunoreactive score (IRS) of apollon protein in glioma tissues was significantly higher than that in the corresponding nonneoplastic brain tissues (P=0.013). Additionally, patients with higher IRS often had advanced World Health Organization (WHO) grade (P=0.001) and shorter overall survival time (P=0.01). Further multivariate analysis identified apollon expression as an independent prognostic factor of glioma patients (P=0.03). Functionally, in vitro experiments revealed that loss of apollon could efficiently suppress migration and invasion of glioma cells.
Conclusions: These findings imply that the dysregulation of apollon may be implicated into tumorigenesis and various pathological changes of human gliomas. Importantly, this protein might be a potential prognostic marker and novel therapeutic target for patients with this tumor.
