chemotherapy to treat GBM is used and the median survival for GBM patients is still about 15 months. Moreover, many of the patients have chemo- and radiotherapy resistance, causing 
very poor prognosis. At this stage, we are not sure about of the glioma pathogenesis; so many researchers have studied on the growth mechanism of malignant gliomas and try to find new effective methods for treatment. Serine/arginine protein kinases family reMedChemExpress Dehydroxymethylepoxyquinomicin present a class of enzymes that can specific bind SR/RS dipeptide motifs, phosphorylate SR splicing factors in cells and mediate splicing factor redistribution during the cell cycle. Human SRPK1, http://www.jcancer.org Journal of Cancer 2013, Vol. 4 the most intensive researched member of this family, is located on chromosome 6p21.2-p21.3, which is expressed in many normal tissues, such as testis and pancreas. SRPK1 has been shown to regulate angiogenesis by interacting with SRSF1 and phosphorylating its RS domain. Phosphorylated SRSF1 is indicative of an angiogenic phenotype as it results in proximal splicing and production of angiogenic VEGF isoforms . It is well known GBM is a highly vascularised tumour, the growth of which needs sufficient oxygen and nutrients from the newly formed blood vessels. The growth of blood vessels is regulated by the the balance between angiogenic factor and anti-angiogenic factor. However, this balance has been destroyed in tumor tissue. The rapid growth of tumor tissue leads to tumor cells living in the state of oxygen hunger and thirst that can prompt hypoxia inducible factor-1 activity and induce high expression of HIF-1 protein. HIF-1 induces the expression level of its downstream target genes, such as vascular endothelial growth factor VEGF. In a present review, here is no report about the expression of SRPK1 in glioma and its performance under the hypoxic condition. PubMed ID:http://www.ncbi.nlm.nih.gov/pubmed/19834673 Here, we found that SRPK1 is expressed in glioma and can promote the growth of U251 cells, even if SRPK1 is present only in neurons and not in glia. More interesting SRPK1 and SRSF1 expression in hypoxic condition can be inhibited and knockdown SRPK1 can inhibit cells invasion, migration and sensitivity to chemotherapy drugs. Also it is significantly higher expressed in low-grade gliomas than in high-grade gliomas, suggesting that SRPK1 as a new molecular player contributing to the early treatment of glioma. 728 made based on the Pathology and Genetics Tumors of Central Nervous System by three pathologists. The clinical information including sex and age was obtained from clinical records. This study was admitted by the Moral and Ethical Committee of the Binzhou Medical University. Western Immunoblotting Cells were washed in PBS and then collected in RIPA lysis buffer for protein quantification followed by addition of sample buffer and then heat denatured at 95C for 10 minutes. Protein lysates were separated using 12% SDS-polyacrylamide gel electrophoresis gels and transferred to Immobilon-P polyvinylidene fluoride membranes. Membranes was blocked with 5% dry non-fat milk, followed by incubation with rabbit Abs against SRPK1 antibody, mouse anti-SF2/ASF, rabbit anti-GAPDH, overnight at 4C. After TBST washing, PVDF membranes were incubated with HRP-conjugated anti-rabbit or anti- mouse IgG Abs for 1h at room temperature. The immune complexes were visualized by enhanced chemiluminescence using an ECL kit, and detected using ChemiScope3400 Mini. Immunohistochemistry and Immunofluorescence For immunohistochemic
