SCLIP, a microtubule-destabilizing phosphoprotein, is known to be involved in the development of the central nervous system (CNS). It has been well established that there are notable parallels between normal development and tumorigenesis, especially in glioma. However, no studies have examined the significance of SCLIP in gliomagenesis. To address this, we investigated the expression of SCLIP and its roles in the development of gliomas. Notably, we found that SCLIP was highly expressed in various grades of glioma samples, as compared with normal brain tissues. Overexpression of SCLIP dramatically stimulated tumor cell migration and invasion as well as proliferation and downregulation of SCLIP showed opposite effects, establishing an important oncogenic role for this gene. Furthermore, we revealed that STAT3 was required to maintain SCLIP stability, suggesting that overexpression of STAT3 may be a critical step to facilitate microtubule dynamics and subsequently promotes migration and invasion of glioma cells. Taken together, our findings demonstrate that SCLIP plays an important role in glioma pathology, and may represent a novel therapeutic strategy against human glioma.
Keywords: BrdU, Bromodeoxyuridine; CHX, cycloheximide; ELISA, enzyme-linked immunosorbent assay; GBM, glioblastoma; HRP, horseradish peroxidase; IHC, immunohistochemical; MTT, 3-[4,5-dimethylthiazol-2-yl] -2,5-diphenyl-tetrazolium bromide; RT-PCR, reversed transcription polymerase chain reaction; SCLIP; SCLIP, SCG10 (superior cervical ganglia protein 10)-like protein Op18, Oncoprotein 18; STAT3; WHO, World Health Organization; glioma; growth; motility; progression; tumorigenesis.