Drosophila lethal (2) giant larvae (lgl) has been reported as a tumor suppressor and could regulate the Drosophila hippo signaling. Human giant larvae-1(Hugl-1), one human homologue of Drosophila lgl, also has been reported to be involved in the development of some human cancers. However, whether Hugl-1 is associated with the pathogenesis of malignant gliomas remains poorly understood. In the present work, we examined the effect of Hugl-1 on glioma cell growth both in vitro and in vivo. Firstly, we found that Hugl-1 protein levels decreased in the human glioma tissues, suggesting that Hugl-1 is involved in glioma progression. Unfortunately, either stably or transiently over-expressing Hugl-1 did not affect glioma cell proliferation in vitro. In addition, Hugl-1 over-expression did not regulate hippo signaling pathway. Interestingly, over-expression of Hugl-1 not only inhibited gliomagenesis but also markedly inhibited cell proliferation and promoted the apoptosis of U251 cells in an orthotopic model of nude mice. Taken together, this study provides the evidence that Hugl-1 inhibits glioma cell growth in intracranial model of nude mice, suggesting that Hugl-1 might be a potential tumor target for glioma therapy.

Objective To assess the expression levels of COTL1 in human GBM tissues and evaluate the potential involvement of COTL1 in cancer progression. Methods Bioinformation analysis was performed to evaluate COTL1 mRNA levels in GBM tissues and normal tissues, according to the TCGA database, and explore the effects on prognosis. Immunohistochemical (IHC) assays were performed to evaluate COTL1 expression in human GBM tissues and the clinical pathological analysis was performed. Colony formation and MTT assays were performed to evaluate the effects of COTL1 on GBM cell proliferation. Immunoblot assays were performed to detect the expression level of COTL1, Ki67, and PCNA. A xenograft model was developed in mice to assess the effects of COTL1 on tumor growth in vivo. Results We found COTL1 had an obvious high expression in human GBM tissues. The expression of COTL1 was related to recurrence ( P =0.006**) and prognosis of patients with GBM. Our data further demonstrated COTL1 promoted cell proliferation in vitro and contributed to tumor growth of GBM cells in mice. Conclusion We therefore identified a novel and promising therapeutic target for the treatment of GBM.

Aim The aim was to study the role of Rph3A in neuronal injury induced by cerebral ischemia‐reperfusion. Methods The protein and mRNA levels of Rph3A in penumbra were detected by Western blot. The localization of Rph3A in different cell types in penumbra was detected by immunofluorescence. Apoptosis in the brain was detected by TUNEL staining. We tested neurobehavioral evaluation using rotarod test, adhesive‐removal test, and Morris Water maze test. We examined the expression and localization of Rph3A in cultured neurons and astrocytes in vitro by Western blot and ELISA, respectively. Results The mRNA and protein levels of Rph3A had significantly increased in brain penumbra of the rat MCAO/R model. Rph3A was mainly distributed in neurons and astrocytes and was significantly increased by MCAO/R. We downregulated Rph3A and found that it further worsened the cerebral infarct, neuronal death and behavioral, cognitive, and memory impairments in rats after MCAO/R. We also found that ischemia‐reperfusion upregulated the in vitro protein level and secretion of Rph3A in astrocytes but led to a decrease in the protein level of Rph3A in neurons. Conclusion The increase in Rph3A in the brain penumbra may be an endogenous protective mechanism against ischemia‐reperfusion injury, which is mainly dominated by astrocytes.