Liensinine ameliorates ischemia-reperfusion-induced brain injury by inhibiting autophagy via PI3K/AKT signaling.

The current study aimed to explore the role of autophagy in cerebral ischemia-reperfusion injuries (CIRI) and elucidate the efficacy of liensinine treatment. An in vitro ischemia-reperfusion (I/R) neuronal cell model was established and pretreated with liensinine or rapamycin (RAPA). Cell proliferation and survival were detected using a cell counting kit-8 (CCK-8) assay, while cell damage and apoptosis were detected using the lactate dehydrogenase (LDH) leakage rate and flow cytometry.

miR-124 suppresses glioblastoma growth and potentiates chemosensitivity by inhibiting AURKA.

Glioblastoma (GBM) accounts for about half of all malignant brain cancers. Although the treatment strategies for glioblastoma develop rapidly, a considerable number of patients could not benefit from temozolomide (TMZ)-based chemotherapy. Here, we revealed a miR-124-AURKA axis that regulated glioblastoma growth and chemosensitivity.

Inhibition of SHP-2 promotes radiosensitivity in glioma.

As a phosphatase, SHP-2 has been identified to be involved in regulating several cell functions, including growth, division, adhesion and motility. Therefore, SHP‑2 may affect the response of glioma to radiotherapy, such as via enhancing angiogenesis. The present study aimed to investigate the function of SHP‑2, a protein tyrosine phosphatase, in the radiosensitivity of glioma.

Stathmin expression in glioma-derived microvascular endothelial cells: a novel therapeutic target.

The purpose of this study was to investigate stathmin expression and its mechanisms of action in GDMEC. Microvascular endothelial cells were isolated from human gliomas (n=68) and normal brain specimans (n=20), and purified by magnetic beads coated with anti-CD105 antibody. The expression of stathmin mRNA and protein were detected by RT-PCR and western blotting, respectively.