Role of CTSC in Glioblastoma Based on Oncomine and TCGA Database

Background and objective Glioblastoma (GBM) is one of the malignant tumors causing death worldwide. Most patients were found in the middle and late stages and had poor prognosis. The purpose of this study was to investigate the expression and significance of CTSC in GBM. Methods The information about CTSC in Oncomine database was collected and analyzed twice. The role of CTSC in GBM was meta-analyzed. The expression of CTSC in glioma cell lines was retrieved by CCLE database, and the survival of patients was analyzed by TCGA database. Results A total of 1,459 different types of CTSC were collected in Oncomine database, 134 of which had statistical differences in CTSC expression, 89 of which had increased CTSC expression and 45 of which had decreased CTSC expression. A total of 50 studies involving the expression of CTSC in GBM cancer and normal tissues included 1,189 samples. Compared with the control group, CTSC was highly expressed in GBM (P < 0.05). Moreover, CTSC was highly expressed in glioma cell lines. There was a correlation between the expression of CTSC and the overall survival rate of GBM. The overall survival rate of patients with high expression of CTSC was worse, while the prognosis of patients with low expression of SPC24 was better (P < 0.05). Conclusion Through the in-depth mining of oncomine gene chip database, we propose that CTSC is highly expressed in GBM tissues and is related to the prognosis of GBM, which may provide an important theoretical basis for the treatment of glioma

The Role of Fluoxetine in Activating Wnt/β-Catenin Signaling and Repressing β-Amyloid Production in an Alzheimer Mouse Model

Fluoxetine (FLX) is one of the selective serotonin reuptake inhibitors (SSRIs) antidepressants, which could be used to relieve depression and anxiety among AD patients. This study was designed to search for new mechanisms by which fluoxetine could activate Wnt/β-catenin signaling pathway and reduce amyloidosis in AD brain. Fluoxetine was administered via intragastric injection to APP/tau/PS1 mouse model of Alzheimer’s disease (3×Tg-AD) mice for 4 months. In the hippocampus of AD mouse model, there could be observed neuronal apoptosis, as well as an increase in Aβ (amyloid-β) production. Moreover, there is a strong association between down-regulation of Wnt/β-catenin signaling and the alteration of AD pathology. The activity of protein phosphatases of type 2A (PP2A) could be significantly enhanced by the treatment of fluoxetine. The activation of PP2A, caused by fluoxetine, could then play a positive role in raising the level of active β-catenin, and deliver a negative impact in GSK3β activity in the hippocampal tissue. Both the changes mentioned above would lead to the activation of Wnt/β-catenin signaling. Meanwhile, fluoxetine treatment would reduce APP cleavage and Aβ generation. It could also prevent apoptosis in 3×Tg-AD primary neuronal cell, and have protective effects on neuron synapse. These findings imply that Wnt/β-catenin signaling could be a potential target outcome for AD prevention, and fluoxetine has the potential to be a promising drug in both AD prevention and treatment