The Chinese Glioma Cooperative Group (CGCG) Guideline Panel for adult diffuse gliomas provided recommendations for diagnostic and therapeutic procedures. The Panel covered all fields of expertise in neuro-oncology, i.e. neurosurgeons, neurologists, neuropathologists, neuroradiologists, radiation and medical oncologists and clinical trial experts. The task made clearer and more transparent choices about outcomes considered most relevant through searching the references considered most relevant and evaluating their value. The scientific evidence of papers collected from the literature was evaluated and graded based on the Oxford Centre for Evidence-based Medicine Levels of Evidence and recommendations were given accordingly. The recommendations will provide a framework and assurance for the strategy of diagnostic and therapeutic measures to reduce complications from unnecessary treatment and cost. The guideline should serve as an application for all professionals involved in the management of patients with adult diffuse glioma and also as a source of knowledge for insurance companies and other institutions involved in the cost regulation of cancer care in China.
Gliomas are the most common type of malignant brain tumors, and the related prognosis is poor. Though many genes have been identified as factors in the development and progression of gliomas, underlying mechanisms remained unclear. It was clear that abnormal lipid metabolism was one of the major hallmarks of cancers. However, few factors associated with lipid metabolism have been reported to be involved in cancer pathogenesis. Hydroxysteroid dehydrogenase-like 2 (HSDL2) is a protein containing sterol carrier protein 2 (SCP2) domain localized in peroxisomes, which indicated that HSDL2 might be a fatty acid regulatory factor. Here, we revealed that HSDL2 was significantly upregulated in gliomas and its expression was positively correlated with glioma grades. Furthermore, lentiviral-mediated HSDL2 knockdown showed that HSDL2 downregulation inhibited the proliferation in two human glioblastoma cell lines U-251 cells and U87 MG cells, induced cell cycle arrest, and promoted cell apoptosis. Our study provided multiple lines of evidence for the causal relationship between HSDL2 overexpression and glioma progression and provided possible mechanisms underlying HSDL2-mediated glioma growth. Taken together, these results indicated that HSDL2 might serve as a potential target for glioma treatment in the future.
Long non-coding RNAs (lncRNAs) have been recently shown to be dysregulated and closely related to several cancers. Here, we aimed to elucidate the function and the possible molecular mechanisms of lncRNA Metastasis-associated lung Adenocarcinoma transcript-1 (MALAT1) in human glioma. Quantitative real-time PCR (qRT-PCR) was used to detect the expressions of MALAT1, miR-101 and Rap1B mRNA in U251 and U87 cells. The protein level of Rap1B was examined by western blot assays. Moreover, the proliferation and apoptosis of U251 and U87 cells were determined by CCK-8 assay and flow cytometry analysis, respectively. Additionally, the targets of miR-101 were identified by target prediction and luciferase reporter assays. The results demonstrated that MALAT1 and Rap1B were upregulated, while miR-101 expression was downregulated in glioma cell lines U251 and U87. MALAT1 and Rap1B knockdown could inhibit proliferation and induce apoptosis of glioma cells. Moreover, MALAT1 promoted the Rap1B expression by sponging miR-101 in U251 and U87 cells. Furthermore, miR-101 downregulation or Rap1B overexpression reversed the proliferation inhibitory and apoptosis induction of glioma cell lines caused by MALAT1 knockdown. Taken together, MALAT1 promotes proliferation and suppresses apoptosis of glioma cells through derepressing Rap1B by sponging miR-101. The present study elucidates a novel MALAT1-miR-101-Rap1B regulatory axis in glioma, contributing to a better understanding of the glioma pathogenesis and providing a promising therapeutic target for glioma patients.
A multifunctional drug delivery system with polypyrrole confined in dendrimer-like silica nanoparticles and DOX loading for chemo-photothermal synergistic therapy of cancer.
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