miR-26b inhibits total neurite outgrowth, promotes cells apoptosis and downregulates neprilysin in Alzheimer's disease.

This study aimed to investigate the effect of miR-26b expression on neurites outgrowth and cells apoptosis in PC12 cellular model of Alzheimer's disease (AD). PC12 cells were stimulated by nerve growth factor and insulted by Aβ to establish PC12 cellular AD model. Methyl thiazolyl tetrazolium (MTT) assay was then used to detect cells viability.

miR-103 Promotes Neurite Outgrowth and Suppresses Cells Apoptosis by Targeting Prostaglandin-Endoperoxide Synthase 2 in Cellular Models of Alzheimer's Disease.

miR-103 has been reported to be decreased in brain of transgenic mouse model of Alzheimer's disease (AD) and in cerebrospinal fluid (CSF) of AD patients, while the detailed mechanism of its effect on AD is obscure, thus this study aimed to investigate the effect of miR-103 expression on neurite outgrowth and cells apoptosis as well as its targets in cellular models of AD. Blank mimic (NC1-mimic), miR-103 mimic, blank inhibitor (NC2-mimic) and miR-103 inhibitor plasmids were transferred into PC12 cellular AD model and Cellular AD model of cerebral cortex neurons which were established by Aβ1-42 insult. Rescue experiment was subsequently performed by transferring Prostaglandin-endoperoxide synthase 2 (PTGS2) and miR-103 mimic plasmid.

MAD2-p31 axis deficiency reduces cell proliferation, migration and sensitivity of microtubule-interfering agents in glioma.

Mitotic arrest deficient-like-1 (MAD2, also known as MAD2L1) is thought to be an important spindle assembly checkpoint protein, which ensures accurate chromosome segregation and is closely associated with poor prognosis in many cancer. As a MAD2 binding protein, p31 counteracts the function of MAD2 and leads to mitotic checkpoint silence. In this study, we explore the function of MAD2-p31 axis in malignant glioma cells.

C-myb Plays an Essential Role in the Protective Function of IGF-1 on Cytotoxicity Induced by Aβ via the PI3K/Akt Pathway.

There have been numerous reports about neurodegenerative diseases, including Alzheimer's disease. Nevertheless, the molecules responsible for the neurodegeneration in Alzheimer's disease are basically unknown. Recent findings indicate that the cellular myeloblastosis (c-myb) regulates neural progenitor cell proliferation.