Receptor tyrosine kinases (RTKs) play an important role in regulating diverse cellular processes, such as proliferation, differentiation, survival, motility, and malignant transformation. The activation of RTKs typically requires ligand-induced receptor oligomerization, which results in tyrosine autophosphorylation of the receptors at tyrosine residues.

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The initial stage of the reaction of oxygen with the surface of layered semiconductor InSe has been studied by XPS. The cleaved surface of InSe does not react with oxygen at room temperature. However, when subjected to Ar ion sputtering, the surface becomes In-rich, and can then be oxidized at room temperature. By heating a sample with a cleaved surface in the atmosphere, the intralayer bonding between Se and In atoms is severed by the formation of In-oxides. In both cases, first, In2O3+x is formed at the surface due to the presence of In–O2 bonds. As oxidation proceeds, In2O3 grows under In2O3+x . In2O3-x is also observed in room-temperature oxidation. No evidence could be found for the presence of Se oxides on the surface under any oxidation conditions. It is found that a heterojunction cell of In2O3–InSe fabricated by the thermal oxidation of InSe exhibits the photovoltaic effect in the visible light region.

The biological and clinical heterogeneity of neuroblastoma is closely associated with signaling pathways that control cellular characteristics such as proliferation, survival and differentiation. The Shc family of docking proteins is important in these pathways by mediating cellular signaling. In this study, we analysed the expression levels of ShcA and ShcC proteins in 46 neuroblastoma samples and showed that a significantly higher level of ShcC protein is observed in neuroblastomas with poor prognostic factors such as advanced stage and MYCN amplification (Po0.005), whereas the expression level of ShcA showed no significant association with these factors. Using TNB1 cells that express a high level of ShcC protein, it was demonstrated that knockdown of ShcC by RNAi caused elevation in the phosphorylation of ShcA, which resulted in sustained extracellular signal-regulated kinase activation and neurite outgrowth. The neurites induced by ShcC knockdown expressed several markers of neuronal differentiation suggesting that the expression of ShcC potentially has a function in inhibiting the differentiation of neuroblastoma cells. In addition, marked suppression of in vivo tumorigenicity of TNB1 cells in nude mice was observed by stable knockdown of ShcC protein. These findings indicate that ShcC is a therapeutic target that might induce differentiation in the aggressive type of neuroblastomas.

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