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.

MicroRNA-16 inhibits glioma cell growth and invasion through suppression of BCL2 and the nuclear factor-κB1/MMP9 signaling pathway.

Recent studies have identified a class of small non-coding RNA molecules, named microRNA (miRNA), that is dysregulated in malignant brain glioblastoma. Substantial data have indicated that miRNA-16 (miR-16) plays a significant role in tumors of various origins. This miRNA has been linked to various aspects of carcinogenesis, including cell apoptosis and migration. However, the molecular functions of miR-16 in gliomagenesis are largely unknown. We have shown that the expression of miR-16 in human brain glioma tissues was lower than in non-cancerous brain tissues, and that the expression of miR-16 decreased with increasing degrees of malignancy. Our data suggest that the expression of miR-16 and nuclear factor (NF)-κB1 was negatively correlated with glioma levels. MicroRNA-16 decreased glioma malignancy by downregulating NF-κB1 and MMP9, and led to suppressed invasiveness of human glioma cell lines SHG44, U87, and U373. Our results also indicated that upregulation of miR-16 promoted apoptosis by suppressing BCL2 expression. Finally, the upregulation of miR-16 in a nude mice model of human glioma resulted in significant suppression of glioma growth and invasiveness. Taken together, our experiments have validated the important role of miR-16 as a tumor suppressor gene in glioma growth and invasiveness, and revealed a novel mechanism of miR-16-mediated regulation in glioma growth and invasiveness through inhibition of BCL2 and the NF-κB1/MMP-9 signaling pathway. Therefore, our experiments suggest the possible future use of miR-16 as a therapeutic target in gliomas.

[Clinic analysis of 16 patients of craniocerebral trauma with Labbé vein injury].

OBJECTIVES: To study the mechanism of Labbé vein injury, and its effect on traumatic cerebral infarction and prognosis in patients of craniocerebral trauma. METHODS: The clinic imageology and data of 16 patients of craniocerebral trauma with Labbé vein injury approved intraoperatively from June 2006 to February 2009 were analyzed. To compare the effect of the intraoperative finding of Labbé vein damage and blood vessel treatment on traumatic cerebral infarction, and to analyze the traumatic cerebral infarction size and prognosis. RESULTS: All the 16 patients had acute subdural hematoma and(or) intracerebral hematoma. And 15 of all the 16 patients with Labbé vein injury suffered from skull fractures. All patients accepted hematoma cleaning and intracranial decompression procedure by removing skull. The preoperative Glasgow coma scale (GCS) were as following: 5 patients being between 9 - 12, 7 patients being between 6 - 8 and 4 patients being between 3 - 5. Eight patients had cerebral hernia before operations on admission, and among them, 3 patients had corectasis of both sides and 5 patients had corectasis of only one side, the other 8 patients had no corectasis. Postoperatively, 14 patients suffered from traumatic cerebral infarction of different grades. After follow-ups of 24 months, 8 patients had relatively good prognosis, with 4 patients having good recoveries and 4 having middle disability; the other 8 had bad prognosis, including 3 patients being seriously disable and 5 kept vegetative state. CONCLUSIONS: Impact injury and counterblow are the main reasons to the injury of Labbé vein, which consequently leads to serious traumatic cerebral infarction and bad prognosis. Intraoperatively, it is quite important to protect Labbé vein during the surgery, which should not be easily cut or obstructed by electric coagulation, and this is an effective way to improve the prognosis of these patients.