Mechanism of RIP2 enhancing stemness of glioma cells induces temozolomide resistance.

Aims: We aimed to investigate the role of receptor-interacting protein 2 (RIP2) in regulation of stemness of glioma cells and chemotherapy resistance.

Methods: Plasmid transfection was used to overexpress RIP2. Chemical inhibitors were used to inhibit RIP2 or NF-κB activity.

Regulation of temozolomide resistance in glioma cells via the RIP2/NF-κB/MGMT pathway.

Background: Temozolomide (TMZ) is a first-line chemotherapy drug for the treatment of malignant glioma and resistance to it poses a major challenge. Receptor-interacting protein 2 (RIP2) is associated with the malignant character of cancer cells. However, it remains unclear whether RIP2 is involved in TMZ resistance in glioma.

Long noncoding RNA OIP5-AS1 targets Wnt-7b to affect glioma progression via modulation of miR-410.

The present study was undertaken to investigate the underlying mechanisms of long noncoding RNA OIP5-AS1 via regulating miR-410 to modulate Wnt-7b in the progression of glioma. To address this problem, we measured the expression of OIP5-AS1 and miR-410 in glioma tissues by qRT-PCR. Glioma U87 cells were transfected with OIP5-AS1 siRNA or miR-410 inhibitors.

Exosomal miR-214-5p Released from Glioblastoma Cells Modulates Inflammatory Response of Microglia after Lipopolysaccharide Stimulation through Targeting CXCR5.

Background And Objective: Exosomes communicate inter-cellularly and miRNAs play critical roles in this scenario. MiR-214-5p was implicated in multiple tumors with diverse functions uncovered. However, whether miR-214-5p is mechanistically involved in glioblastoma, especially via exosomal pathway, is still elusive.

Delayed cognitive deficits can be alleviated by calcium antagonist nimodipine by downregulation of apoptosis following whole brain radiotherapy.

Radiation therapy is important for the comprehensive treatment of intracranial tumors. However, the molecular mechanisms underlying the pathogenesis of delayed cognitive dysfunction are not well-defined and effective treatments or prevention measures remain insufficient. In the present study, 60 adult male Wistar rats were randomly divided into three groups, which included a control, whole brain radiotherapy (WBRT) (single dose of 30 Gy of WBRT) and nimodipine (single dose of 30 Gy of WBRT followed by nimodipine injection intraperitoneally) groups.

DNM3, p65 and p53 from exosomes represent potential clinical diagnosis markers for glioblastoma multiforme.

Background: Glioblastoma multiforme (GBM) is the most aggressive and deadly primary brain cancer that arises from astrocytes and classified as grade IV. Recently, exosomes have been reported as an essential mediator in diverse cancer carcinogenesis and metastasis. However, their role in GBM is still unclear.

Downregulation of ZMYND11 induced by miR-196a-5p promotes the progression and growth of GBM.

ZMYND11 (zinc finger MYND-type containing 11) has been widely regarded to be involved in a variety of cancers as a potential suppressor. However, the biological role and mechanism of ZMYND11 in glioblastoma multiform (GBM) remain unknown. In this study, we found that ZMYND11 expression was remarkably decreased in GBM tissues from 20 cases and cell line (U87) compared to normal brain tissue from 10 cases (P < 0.

miR-133a Promotes TRAIL Resistance in Glioblastoma via Suppressing Death Receptor 5 and Activating NF-κB Signaling.

Recombinant tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL), as a novel cancer therapeutic, is being tested in phase II and III clinical trials; however, TRAIL resistance remains a big obstacle preventing its clinical application. Considering that TRAIL-induced apoptosis through death receptors DR4 and DR5, their activation may be an alternative pathway to suppress TRAIL resistance. In this study, a negative correlation between DR5 expression and TRAIL resistance was observed, and miR-133a was predicted to be the most promising candidate to suppress DR5 expression.

Exosomal miR-221 targets DNM3 to induce tumor progression and temozolomide resistance in glioma.

MicroRNA is an important regulator of glioblastoma. This study aims at validating microRNA-221 (miR-221) as a biomarker for glioblastoma, and understanding how miR-221 regulates glioblastoma progression. Using clinical samples, miR-221 expression was analyzed by quantitative reverse-transcriptase PCR (qPCR).

Downregulation of miR-95-3p inhibits proliferation, and invasion promoting apoptosis of glioma cells by targeting CELF2.

Gliomas are the most common and aggressive types of tumors in human brain, of which the prognosis remains dismal because of their biological behavior. The involvement of miRNAs in tumorigenesis of various kinds of cancers drives us to explore new miRNAs related to gliomas. We measured expression level of miR‑95‑3p by qRT-PCR in human glioma and non-neoplasm brain tissues and found that higher level of miR‑95‑3p in glioma tissues of higher grade.

High expression of forkhead box protein C2 is related to poor prognosis in human gliomas.

Background: Increasing evidence has indicated that high Forkhead box protein C2 (FOXC2) level is closely associated with the development, progression, and poor prognosis of a variety of tumors. However, the relationship between FOXC2 and the progression of human gliomas remains to be clarified. The aim of present study was to assess FOXC2 expression and to explore its contribution in human gliomas.

Over-expression of wild-type p53-induced phosphatase 1 confers poor prognosis of patients with gliomas.

Wild-type p53-induced phosphatase 1 (Wip1) is a member of the protein phosphatase 2C family, which is characterized by distinctive oncogenic properties. Overexpression of Wip1 is observed in certain types of human tumors that are associated with significantly poor prognosis. This study aimed to detect the expression of Wip1 in gliomas and to analyze its prognostic value in the patients.

[The inhibition of tamoxifen on sodium channel in SHG-44 glioma cell-line].

Aim: To explore the effect of tamoxifen on voltage-dependent sodium channels in SHG-44 glioma cell line.

Methods: Whole-cell patch clamp technique was used to record the Na currents in SHG-44 cell line and to investigate the effect of tamoxifen of different concentration on this channel currents.

Results: This channel activated and inactivated quickly.

[Correlations of polymorphisms in matrix metalloproteinase-3 and -7 promoters to susceptibility to brain astrocytoma].

Background & Objective: Matrix metalloproteinases (MMPs) are key enzymes involved in tumor development, invasion and metastasis. The single nucleotide polymorphisms (SNPs) in the promoter regions of MMP genes may influence tumor development and progression via modulating mRNA transcription and protein expression. This study was to explore the correlations of the promoter SNPs in MMP-3 and MMP-7 genes to susceptibility to brain astrocytoma.

[Anti-glioma activity of treatment by bone marrow stromal cells transfected with HSV-tk in the rat].

Objective: To study the anti-glioma activity of treatment by bone marrow stromal cells (BMSCs) transfected with AdCMV-tk containing HSV-tk gene in rats.

Methods: Primary cultured BMSCs were obtained and transfected with HSV-tk (BMSCs/tk) and were injected into contralateral brain of glioma-bearing rats to observe their tropism for glioma cells. RT-PCR was performed to examine the transduct of tk gene after it was transduced into BMSCs.

[Effect of bone marrow stromal cells transfected with interleukin 18 on growth of intracranial glioma in rats].

Background & Objective: Because of the invasion and immune escape characteristics, surgical resection, radiotherapy, and chemotherapy had no definite curative effects on intracranial glioma. Because bone marrow stromal cells (BMSCs) can track migrating cells, and interleukin 18 (IL-18) can enhance antitumor immune reaction, this study was to explore the effect of IL-18-transfected BMSCs on growth of glioma in rats.

Methods: Pure BMSCs were obtained by culturing rat bone marrow cells and identified by flow cytometry (FCM).

[Preliminary analysis on the gene expression profiles of medulloblastomas by use of cDNA array].

Objective: To explore the molecular genesis of medulloblastomas with cDNA array.

Methods: Four samples of medulloblastomas and 1 sample of normal brain tissue were collected freshly. After total RNA extraction, the (32)P targeted cDNA probes were converted and then hybridized with Atlas Human Cancer Array 1.

[Preliminary study on the gene expression profiles of ependymomas with cDNA array].

Objective: To investigate the differential gene expression of ependymomas.

Methods: Four fresh samples of ependymomas and 1 of normal brain tissue were collected during operation. The extracted total RNAs were converted as (32)P tagged cDNA probes, which were then hybridized with the Atlas Human Cancer Array, producing the array based hybridization maps following the protocol provided with the kit.

[Preliminary analysis on the gene expression profiles of different types of gliomas with cDNA array].

Background & Objective: There is great signification to classify the molecular pathogenesis of gliomas. Gene chip is able to profile the gene expression of tumors, which may become a new method for studying molecular pathology of tumors. The cDNA was used in order to detect the differences in gene expression profiles of different types of gliomas.