Original Article
Expression of centrosomal protein 55 in glioma tissue and the influence on glioma cell functions
Abstract
Background: Centrosomal protein 55 (CEP55) protein has high expression levels in various tumors and plays important regulatory effects on cell cycle. We aimed to detect the expressions of CEP55 in glioma tissues, and to evaluate the effects on glioma cell functions and apoptosis.
Methods: Fifty fresh astrocytoma tissue samples resected from surgeries were collected, and twenty normal brain tissue samples were obtained as a control group. CEP55 protein expressions were measured by Western blot and immunohistochemical assay. After siRNA interference, the proliferation, migration, invasion and apoptosis of glioma cell lines LN229/T98G were detected by MTT assay, scratch assay, Transwell assay and flow cytometry respectively.
Results: The expression level of CEP55 protein in glioma tissue was significantly higher than that in normal control group, and the expressions in glioma tissues were elevated with increasing grade. Glioma cell lines in which CEP55 expression was stably knocked down were successfully constructed. MTT assay showed that the growth of these cells was significantly slowed down compared with that of normal cells. Scratch assay exhibited that their migration capability significantly decreased. Transwell assay revealed that the invasive ability was also attenuated with decreasing CEP55 expression. Flow cytometry showed that down-regulated expression of CEP55 promoted the apoptosis of LN229/T98G cells.
Conclusions: CEP55 expression increased in glioma tissues. After interference of its expression, glioma cell functions were significantly weakened, and apoptosis was facilitated. CEP55 may be a molecular marker for glioma diagnosis or a new target for molecular therapy.
Methods: Fifty fresh astrocytoma tissue samples resected from surgeries were collected, and twenty normal brain tissue samples were obtained as a control group. CEP55 protein expressions were measured by Western blot and immunohistochemical assay. After siRNA interference, the proliferation, migration, invasion and apoptosis of glioma cell lines LN229/T98G were detected by MTT assay, scratch assay, Transwell assay and flow cytometry respectively.
Results: The expression level of CEP55 protein in glioma tissue was significantly higher than that in normal control group, and the expressions in glioma tissues were elevated with increasing grade. Glioma cell lines in which CEP55 expression was stably knocked down were successfully constructed. MTT assay showed that the growth of these cells was significantly slowed down compared with that of normal cells. Scratch assay exhibited that their migration capability significantly decreased. Transwell assay revealed that the invasive ability was also attenuated with decreasing CEP55 expression. Flow cytometry showed that down-regulated expression of CEP55 promoted the apoptosis of LN229/T98G cells.
Conclusions: CEP55 expression increased in glioma tissues. After interference of its expression, glioma cell functions were significantly weakened, and apoptosis was facilitated. CEP55 may be a molecular marker for glioma diagnosis or a new target for molecular therapy.
