Loss of GINS2 inhibits cell proliferation and tumorigenesis in human gliomas.

Aims: In this study, we examined the expression of GINS2 in glioma and determined its role in glioma development.

Methods: The protein expression of GINS2 was assessed in 120 human glioma samples via immunohistochemistry. Then, we suppressed the expression of GINS2 in glioma cell strains U87 and U251 using a short hairpin RNA lentiviral vector.

[MACF1 knockdown in glioblastoma multiforme cells increases temozolomide-induced cytotoxicity].

Objective: To investigate the role of microtubule-actin crosslinking factor 1 (MACF1) in the response of glioma cells to temozolomide (TMZ).

Methods: TMZ was applied to a human gliomablastoma cell line (U87) and changes in the protein expression and cellular localization were determined with Western blot, RT-PCR, and immunofluorescence. The responses of the cells with MACF1 expression knockdown by RNA interference to TMZ were assessed.

Differences in Protein Expression between the U251 and U87 Cell Lines.

Aim: The U251 and U87 cell lines are commonly used as experimental models of glioblastoma. However, these cells exhibit significant differences in their proliferation, invasion, and migration. The aim of the present study was to compare the protein expression profiles of the U251 and U87 cell lines in order to provide a molecular basis for the observed phenotypic differences.

Expression of dynein, cytoplasmic 2, heavy chain 1 (DHC2) associated with glioblastoma cell resistance to temozolomide.

Temozolomide (TMZ) is the main chemotherapeutic drug utilized for the treatment of glioblastoma multiforme (GMB), however, drug resistance often leads to tumor recurrence and poor outcomes. GMB cell lines were treated with TMZ for up to two weeks and then subjected to proteomics analysis to identify the underlying molecular pathology that is associated with TMZ resistance. Proteomics data showed that TMZ altered expression of proteins that related to cytoskeleton structure and function, such as DHC2 and KIF2B.

[RNA interference of PC4 and SFRS1 interacting protein 1 inhibits invasion and migration of U87 glioma cells].

Objective: To investigate the effect of small interfering RNA (siRNA)-mediated silencing of PC4 and SFRS1 interacting protein 1 (PSIP1) on invasion and migration of human glioma U87 cells.

Methods: Chemically synthesized siRNA targeting PSIP1 gene was transfected into U87 cells via lipofectamine, and the gene silencing effect was determined using real-time PCR. The changes in the invasion and migration abilities of the transfected cells were assessed with Transwell assay and wound healing assay, respectively.

Inhibition of EZH2 reverses chemotherapeutic drug TMZ chemosensitivity in glioblastoma.

Glioblastoma remains among the most devastating cancers with a median survival of less than 15 months and virtually no survival beyond five years. Currently, the treatment of glioma includes surgery, radiation therapy, chemotherapy, and comprehensive treatment. Intrinsic or acquired resistance to TMZ, is one of the greatest obstacles in successful GB treatment, and is thought to be influenced by a variety of mechanisms.

Isocitrate dehydrogenase mutation is associated with tumor location and magnetic resonance imaging characteristics in astrocytic neoplasms.

The molecular subsets of glioma behave in biologically distinct ways. The present study detected isocitrate dehydrogenase ) 1 and mutations in glioma to analyze whether -mutated gliomas are situated in certain preferential areas and to investigate their correlation with magnetic resonance imaging (MRI) characteristics. A series of 193 patients with astrocytic neoplasms (111 diffuse and 82 anaplastic astrocytomas), grouped according to prelabeled anatomical structures and the risk of surgery, were retrospectively reviewed for 1 and 2 mutations to compare the tumor location and MRI features.