In summary, we demonstrated that miR-16-1 expression was markedly decreased in human glioma cell lines, and for the first time, described the roles of miR-16-1 in cellular proliferation, migration, and invasion abilities of high-invasive glioma cells, and suggested that Zyxin may be one of putative target genes of miR-16-1.
Neither baseline p27 levels nor p27 levels induced by confluency or serum deprivation correlate with p53 status or drug sensitivity of human glioma cell lines.
Mechanically, salinomycin-induced cell growth inhibition against human glioma was mainly achieved by induction of G1-phase arrest via triggering reactive oxide species (ROS)-mediated DNA damage, as convinced by the activation of histone, p53, p21 and p27.
Thus, disrupted regulation of p27 expression at high cell density may play an important role in determining the clinical behavior of human gliomas as well as the prognosis for glioma patients.
This study assessed whether CRM1, Ser10-phosphorylated p27, and p27 correlated with each other, with glioma pathological stage, and with patient outcome.
It was investigated whether there was a relationship between p53 p21 and p27 induction pathways in the cellular response of glioma cells to hyperthermia.Two glioma cell lines were employed.
Immunohistochemistry was applied to detect the expression of ZNF326 in glioma tissues, and statistical analysis was used to analyse the relationship between ZNF326 expression and clinicopathological factors.
ZNF342 expression is specifically decreased in primary oligodendrogliomas and up-regulated in glioma cell lines treated with a demethylating agent, whereas the expression level of the adjacent gene, Gemin7, is not consistently altered in these samples.
Our data demonstrates that lncRNA-ZNF281 inhibits the self-renewing ability and invasion of GSCs in vitro and in vivo and can reduce tumorigenicity in the glioma stem-like cell (U251s).
Therefore, in glioma cells, circ-ZNF264 can inhibit the function of miR-4493 and then upregulate its target gene apelin expression, thus regulating glioma cell proliferation, apoptosis, and invasion.
Quantitative RT-PCR and western blotting of a cohort of glioma samples showed that ZNF217 was highly expressed in gliomas and increased with tumor grade.
The present study clarifies that the A1CF-FAM224A-miR-590-3p-ZNF143 positive feedback loop conducts critical regulatory effects on the malignant progression of glioma cells, which provides a novel molecular target for glioma therapy.
Ninety-two percent of tumor samples were methylated for RASSF1A, 30%-57% for BLU and 47% for MGMT, suggesting promoter methylation of these genes to be a common event in glioma tumorigenesis.
The study is the first to prove that the UPF1-Linc-00313-miR-342-3p/miR-485-5p-Zic4-SHCBP1 pathway forms a positive-feedback loop and regulates the biological behaviors of U87 and U251 cells, which might provide a new therapeutic target for glioma.
We also summarize clinical experience with RAF and MEK inhibitors in patients with primary brain tumors and describe ongoing clinical trials of RAF inhibitors in glioma.