Synthesis and Growth Mechanism of SiS2 Rods.

The SiS2 rods exhibit a significant anisotropy property applied in a special field such as in the one of all-solid-state lithium-ion batteries and so on. In this work, the orthorhombic SiS2 rods with high chemical/phase purity were prepared by an elemental method, either through a boiling or a steaming process, at 1023-1073 K for 3 h and under the saturated S-vapor pressure (2.57-3.83 MPa) in a closed sealed-tube system. The composition, crystal structure, morphology, and growth mechanism were investigated. Results showed that the growth orientation of SiS2 along the <0 0 1> is intrinsically governed by the crystal structure motif. It could exist in both processes and the latter tends to show in macroscopic morphology. Using the pressure-temperature diagram, structure refinement, pole figures, image analyses, and so forth, factors influencing the purity and growth of SiS2 rods were concluded from the thermodynamics and kinetics viewpoints.

SH2B3, Transcribed by STAT1, Promotes Glioblastoma Progression Through Transducing IL-6/gp130 Signaling to Activate STAT3 Signaling.

Glioblastoma (GBM) is the most common and aggressive brain tumor in adults. The aberrant activation of STAT3 commonly occurs in GBM and is a key player in GBM tumorigenesis. Yet, the aberrant activation of STAT3 signaling is not fully understood. Here, we report that SH2B adaptor protein 3 (SH2B3) is highly expressed in GBM and preferentially expressed in GBM stem cells (GSCs). Moreover, SH2B3 high expression predicts worse survival of GBM patients. Targeting SH2B3 considerably impairs GBM cell proliferation, migration, and GSCs' self-renewal in vitro as well as xenograft tumors growth in vivo. Additionally, we provide evidence suggesting that STAT1 directly binds to the promoter of SH2B3 and activates SH2B3 expression in the transcriptional level. Functionally, SH2B3 facilitates GBM progression via physically interacting with gp130 and acting as an adaptor protein to transduce IL-6/gp130/STAT3 signaling. Together, our work firstly uncovers that the STAT1/SH2B3/gp130/STAT3 signaling axis plays critical roles in promoting GBM progression and provides insight into new prognosis marker and therapeutic target in GBM.

miR­124­3p inhibits the viability and motility of glioblastoma multiforme by targeting RhoG.

The mortality rate of patients with glioma is increasing worldwide per annum. This is attributed to the poor disease prognosis, most notably for high­grade gliomas (grade III and IV), which does not improve the overall patient survival. The dysregulation of microRNA (miRNA/miR)­124­3p is found in a variety of tumors. However, the association between miR­124­3p expression and its target genes in glioma has not been thoroughly elucidated. The present study aimed to explore the possible effects of miR­124­3p and its proved target, Ras homology Growth­related (RhoG), on the oncogenic events associated with glioblastoma multiforme (GBM) development. The data demonstrated an inverse association between miR­124­3p and RhoG expression levels during GBM progression in GBM tissues and cells. U87 and U251 cells were employed for the in vitro assays. Luciferase reporter assays revealed that miR­124­3p interacted with RhoG at the RhoG 3' untranslated region and inhibited RhoG expression in GBM cells. Functionally, enriched miR­124­3p repressed RhoG transcription and suppressed GBM cell proliferation and migration, promoting apoptosis and altering the expression or activity of the apoptosis­related proteins of GBM cells. By contrast, the inhibition of miR­124­3p in GBM cells upregulated RhoG levels and promoted the proliferation of GBM cells. The knock down of RhoG expression by specific small interfering RNA sequences partially neutralized the effects induced by the miR­124­3p inhibitor. In conclusion, the present study demonstrated the crucial effects of miR­124­3p on the development and deterioration of GBM by targeting RhoG.