Glioma has been investigated for decades, but the prognosis remains poor because of rapid proliferation, its aggressive potential, and its resistance to chemotherapy or radiotherapy. The mammalian target of rapamycin (mTOR) is highly expressed and regulates cellular proliferation and cell growth. MicroRNAs (miRNAs) are small non-coding RNAs that regulate gene transcription and translation via up-regulating or down-regulating the levels of miRNAs. This study was conducted to explore the molecular functions of miR-199a-3p in glioma. We detected the expression of miR-199a-3p in glioma samples by quantitative PCR (qPCR). Then, we transfected the U87 and U251 cell lines with miR-199a-3p. Cellular proliferation, invasion, and apoptosis were assessed to explain the function of miR-199a-3p. PCR confirmed that the expression of miR-199a-3p was lower in glioma samples combined with normal brain tissues. The over-expression of miR-199a-3p might target mTOR and restrained cellular growth and proliferation but not invasive and apoptosis capability. Results indicated that cellular proliferation was inhibited to regulate the AKT/mTOR signaling pathway by elevating levels of miR-199a-3p. MiR-199a-3p in glioma cell lines has effects similar to the tumor suppressor gene on cellular proliferation via the AKT/mTOR signaling pathway.

Spalt-like transcription factor 4 (SALL4), a oncogene, is known to participate in multiple carcinomas, and is up-regulated in glioma. However, its actual role and underlying mechanisms in the development of glioma remain unclear. The present study explored the molecular functions of SALL4 in promoting cell proliferation in glioma. The expression level of SALL4 in 69 human glioma samples and six non-tumor brain tissues was determined using real-time polymerase chain reaction (PCR). Then, we transfected U87 and U251 cell lines with siRNA, and assessed cellular proliferation and cell cycle to understand the function of SALL4, and the relationship between SALL4, PTEN and PI3K/AKT pathway. PCR confirmed that the expression of SALL4 was higher in the glioma samples than non-tumor brain tissues. Cellular growth and proliferation were dramatically reduced following inhibition of SALL4 expression. Western blot showed increase in PTEN expression when SALL4 was silenced, which in turn depressed the activation of PI3K/AKT pathway, suggesting that PTEN was a downstream target of SALL4 in glioma development. Therefore, SALL4 could act as a proto-oncogene by regulating the PTEN/PI3K/AKT signaling pathway, thereby facilitating proliferation of glioma cells.

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The present-day kinematic features of the different segments of the Altyn Tagh Fault (ATF) have been well-studied using geodetic data. However, on the eastern segment of the ATF at 91.5-95 • E, high spatial resolution deformation has not been previously reported. Here, we processed 185 interferometric synthetic aperture radar (InSAR) images from three descending tracks of the C band ERS-1/2 and Envisat satellites spanning 1995-2011 and obtained the average deformation velocity field. Results show a left-lateral motion of~4 mm/year along the fault-parallel direction across the ATF at 91.5-95 • E, which is consistent with Global Positioning System (GPS) observations. The slip deficit rate distribution at shallow depths was resolved through the InSAR deformation velocity using a discretized fault plane. The slip deficit is capable of an Mw 7.9 earthquake, considering the elapsed time of the latest M 7.0 event. Two potential asperities that could be nucleation sites or rupture areas of future earthquakes were delineated based on the coupling coefficient and seismicity distributions along the fault plane. The larger asperity extends more than 100 km along the ATF at depths of 8-12 km. Our InSAR observations support the undeformed blocks model of the Indo-Eurasian collisional mechanism at the northern margin of the Tibetan plateau.