miR-494-3p Regulates Cellular Proliferation, Invasion, Migration, and Apoptosis by PTEN/AKT Signaling in Human Glioblastoma Cells.

Malignant gliomas are the most common primary brain tumors, and the molecular mechanisms involving their progression and recurrence are still largely unclear. Substantial data indicate that the oncogene miR-494-3p is significantly elevated in gliomas, but the molecular functions of miR-494-3p in gliomagenesis are largely unknown. The present study aimed to explore the role of miR-494-3p and its molecular mechanism in human brain gliomas, malignant glioma cell lines, and cancer stem-like cells. The expression level of miR-494-3p in 48 human glioma issues and 8 normal brain tissues was determined using stem-loop real-time polymerase chain reaction (PCR). To study the function of miR-494-3p inhibitor in glioma cells, the miR-494-3p inhibitor lentivirus was used to transfect glioma cells. Transwell invasion system was used to estimate the effects of miR-494-3p inhibitor on the invasiveness of glioma cells. A mouse model was used to test the effect of miR-494-3p inhibitor on glioma proliferation and invasion in vivo. Results showed that the expression of miR-494-3p in human brain glioma tissues was higher than in normal brain tissues. Downregulated expression of miR-494-3p can inhibit the invasion and proliferation and promote apoptosis in glioma cells. Quantitative reverse transcription PCR and Western blotting analysis revealed that the expression of PTEN was increased after downexpression of miR-494-3p in glioma cells (U87 and U251). miR-494-3p inhibitor could prevent migration, invasion, proliferation, and promote apotosis in gliomas through PTEN/AKT pathway. Therefore, the study results have shown that miR-494-3p may act as a therapeutic target in gliomas.

[Binding mechanism of rhaponticin and human serum albumin].

The interaction mechanism between rhaponticin (RT) and human serum albumin (HSA) has been studied by fluorescence spectroscopy and absorbance spectra. The mediation effect that the metal ions took part in the interaction has also been discussed in this paper. Based on different theoretical models of fluorescence quenching, the binding constant (K) and binding sites (n) of the interaction were determined and analyzed comparatively. The quenching mechanism of the binding reaction has also been discussed. The binding distance (r) and energy-transfer efficiency (E) between RT/RT-Co(II)/RT-Ni(II) and HSA were also obtained by virtue of the Förster theory of non-radiation energy transfer. The effect of RT acting on the HSA's conformation was analyzed by synchronous fluorescence spectroscopy. The result showed that the result calculated by different theoretical models is generally equivalent and RT bound HSA strongly by forming stable complex, which indicates that HSA under physiological conditions can act as a carrier for RT to be transported to exert effects. The microconformation of HSA changed significantly due to hydrophobicity change in the chemical environment of some fluorescence chromophores in the subdomain IIA and IIB of HSA. Metal ions Co(II) and Ni(II) can mediate RT-HSA interaction, making the binding of the drug to protein stronger, which indicates that Co(II) and Ni(II) can enhance rhaponticin's medical efficacy under physiological conditions.

miR-132 can inhibit glioma cells invasion and migration by target MMP16 in vitro.

Gliomas are the most common malignant primary brain tumors, and new clinical biomarkers and therapeutic targets are imminently required. MicroRNAs (miRNAs) are a novel class of small non-coding RNAs (∼22nt) involved in the regulation of various biological processes. Here, by using real-time polymerase chain reaction, miRNA-132 was found to be significantly deregulated in glioma tissues. Based on the prediction of the target genes of miR-132, we hypothesized that there is a significant association between miR-132 and matrix metalloproteinase (MMP) 16 (MT3-MMP), a protein of the MMP family. We showed that the up-expression of miR-132 inhibited cell migration and invasion in the human glioma cell lines A172, SHG44, and U87. Furthermore, the overexpression of miR-132 reduced the expression of MMP16 in A172, SHG44, and U87 cells. Taken together, our study suggested that miR-132 affects glioma cell migration and invasion by MMP16 and implicates miR-132 as a metastasis-inhibiting miRNA in gliomas.