Investigating the results of neuroendoscopic surgery in the treatment of pituitary adenoma and leptin gene expression.

Neuroendoscopic surgery of pituitary adenoma has been one of the technologies with rapid progress in neurosurgery in this decade. This method has known advantages and limitations. This study aims to investigate the results of pituitary adenoma treatment using the neuroendoscopy technique in a group of patients. Also, the level of leptin gene expression (LEP), which is produced exclusively in the pituitary gland, was measured for further evaluation. For this purpose, 26 patients who were diagnosed with pituitary adenoma and underwent endoscopic surgery in the hospital between 2018-2022, in terms of age, gender, disease symptoms, functional and non-functional tumor, and neurological examination findings before and after the procedure, complications, and the length of stay in the hospital were investigated. Also, before and 6 months after the operation, blood samples were prepared from patients to evaluate LEP gene expression by real-time PCR technique. The results illustrated that of the 26 patients studied, 14 were men, and 12 were women. Most of the patients were in their third to sixth decades of life. The tumors were non-functioning adenoma in 11 cases, somatotroph adenoma in 9 patients, corticotroph adenoma in 3 cases, and prolactinoma in 3 cases. Seven patients suffered postoperative complications, including 6 cases of reversible complications and one case of patient death. In the 2-year follow-up, 6 cases of tumor recurrence were observed. Also, the evaluation of LEP gene expression showed no significant difference between pre-operative and post-operative expressions. In general, neuroendoscopic surgery in treating pituitary adenoma is a method worthy of attention, considering factors such as fewer complications and a shorter stay in the hospital increase the acceptability of this method.

Inhibition of PLK4 might enhance the anti-tumour effect of bortezomib on glioblastoma via PTEN/PI3K/AKT/mTOR signalling pathway.

Glioblastoma (GBM) is one of the most common aggressive cancers of the central nervous system in adults with a high mortality rate. Bortezomib is a boronic acid-based potent proteasome inhibitor that has been actively studied for its anti-tumour effects through inhibition of the proteasome. The proteasome is a key component of the ubiquitin-proteasome pathway that is critical for protein homeostasis, regulation of cellular growth, and apoptosis. Overexpression of polo-like kinase 4 (PLK4) is commonly reported in tumour cells and increases their invasive and metastatic abilities. In this study, we established a cell model of PLK4 knockdown and overexpression in LN-18, A172 and LN-229 cells and found that knockdown of PLK4 expression enhanced the anti-tumour effect of bortezomib. We further found that this effect may be mediated by the PTEN/PI3K/AKT/mTOR signalling pathway and that the apoptotic and oxidative stress processes were activated, while the expression of matrix metalloproteinases (MMPs) was down-regulated. Similar phenomenon was observed using in vitro experiments. Thus, we speculate that PLK4 inhibition may be a new therapeutic strategy for GBM.

Casein Kinase 2 Interacting Protein-1 Suppresses Glioma Cell Proliferation via Regulating the AKT/GSK3ß/ß-Catenin Pathway.

OBJECTIVE: Casein kinase 2 interacting protein-1 (CKIP-1) has exhibited multiple functions in regulating cell proliferation, apoptosis, differentiation, and cytoskeleton. CKIP-1 also plays an important role as a critical regulator in tumorigenesis. The aim of this study is to further examine the function of CKIP-1 in glioma cells. METHODS: The expression level of CKIP-1 protein was determined in gliomas tissues and cell lines by immunohistochemistry stain and western blotting while the association of CKIP-1 expression with prognosis was analyzed by Kaplan-Meier method and compared by log-rank test. CKIP-1 was overexpressed or silenced in gliomas cell lines. CCK-8, colony formation assay, and BrdU incorporation assay were used to determine cell proliferation and DNA synthesis. Cell cycle and apoptosis rate were determined with fluorescence-activated cell sorting (FACS) method. Then, expression of key members in AKT/GSK3ß/ß-catenin pathway was detected by western blot analysis. RESULTS: In the present study, we reported new evidence that CKIP-1 was reversely associated with the proliferation of glioma cells and survival in glioma patients. Additionally, the overexpressed CKIP-1 significantly inhibited glioma cell proliferation. Further experiments revealed that CKIP-1 functioned through its antiproliferative and proapoptotic activity in glioma cells. Importantly, mechanistic investigations suggested that CKIP-1 sharply suppressed the activity of AKT by inhibiting the phosphorylation, markedly downregulated the phosphorylated GSK3ß at Ser9, and promoted ß-catenin degradation. CONCLUSIONS: Overall, our results provided new insights into the clinical significance and molecular mechanism of CKIP-1 in glioma, which indicated CKIP1 might function as a therapeutic target for clinical treatment of glioma.