Glioma is the most common and lethal type of primary brain tumor, with a high mortality and recurrence rate. Rab5, which serves as a classic ontogenetic gene, is highly expressed in various types of tumor, including lung cancer, hepatocellular carcinoma and ovarian cancer. However, the exact role and the underlying mechanism of Rab5 in glioma remain unknown. Herein, the role of Rab5 in the tumorigenesis and metastasis of glioma cells was investigated. The upregulation of Rab5 in glioma tissues and cells was observed. The expression of Rab5 was positively associated with proliferation, migration and invasion of glioma cells. Moreover, Rab5 was involved in the cell cycle of glioma cells via the regulation of cyclin E. Data presented in the present study suggest Rab5 as a potential novel diagnostic and prognosis marker of glioma.

Doxorubicin (DOX) is an anthracycline anticancer drug, which is often associated with drug resistance and cytotoxicity. More unfortunately, the biological barrier in the human environment can weaken the efficacy of DOX, such as the blood-brain barrier (BBB). This work attempts to make efforts to solve this problem. We used polyethylene glycol distearoylphosphatidylethanolamine (PEG-DSPE) as a nanocarrier and DOX as a model drug to construct a composite nanodrug (TF-PEG-DSPE/DOX NPs) by coupling transferrin (TF). The results of glioma experiments show that the nanodrug can effectively penetrate BBB to achieve an antitumor effect.

Objective The study is designed to observe the influence of LncRNA LINC00152 on the proliferation of glioma cells and explore the role of Src-YAP signal pathway in the process.Methods U251 and U87 cell were used for in vitro experiments and xenograft studies; transfection method was adopted to build a LINC00152 overexpressing cell strain, and cell viability was determined by MTT assay; cell colony formation ability was measured through colony formation assay, and protein expression was determined by Western blot; YAP protein expression distribution is detected through Immunofluorescence.Key findings LINC00152 overexpressing can enhance the U251 and U87 cell proliferation, the colony formation and the growing ability of subcutaneously transplanted tumor, and it induces YAP nuclear import and down-regulates p-LATS1 and p-YAP protein expression, and up-regulates p-Src protein expression. Src inhibitor 1 can inhibit the changes in protein expression and the cell colony formation of p-LATS1, p-YAP and p-Src, which are induced by overexpression of LINC00152 in U251 and U87 cells.Conclusions LINC00152 promotes cell proliferation of glioma U251 and U87, and the action might be associated with process of activation of Src, inhibition of phosphorylation cascade reaction of LATS1-YAP pathway and final inducing of YAP nuclear import.