PO4 3- Coordinated Robust Single-Atom Platinum Catalyst for Selective Polyol Oxidation.

Achieving efficient catalytic conversion over a heterogeneous catalyst with excellent resistance against leaching is still a grand challenge for sustainable chemical synthesis in aqueous solution. Herein, we devised a single-atom Pt1 /hydroxyapatite (HAP) catalyst via a simple hydrothermal strategy. Gratifyingly, this robust Pt1 /HAP catalyst exhibits remarkable catalytic selectivity and catalyst stability for the selective oxidation of C2 -C4 polyols to corresponding primary hydroxy acids. It is found that the Pt-(O-P) linkages with strong electron-withdrawing function of PO4 3- (Pt1 -OPO4 3- pair active site) not only realize the activation of the C-H bond, but also destabilize the transition state from adsorbed hydroxy acids toward the C-C cleavage, resulting in the sharply increased selectivity of hydroxy acids. Moreover, the strong PO4 3- -coordination effect provides electrostatic stabilization for single-atom Pt, ensuring the highly efficient catalysis of Pt1 /HAP for over 160 hours with superior leaching resistance.

c-Myc induced upregulation of long non-coding RNA SNHG16 enhances progression and carcinogenesis in oral squamous cell carcinoma.

Small nucleolar RNA host gene 16 (SNHG16) has been documented to be involved in the pathogenesis of human cancers. Here, we elucidated the biological roles and regulatory mechanism of SNHG16 in the pathogenesis of oral squamous cell carcinoma (OSCC). In this paper, we found that c-Myc and SNHG16 were overexpressed in OSCC tissues and cell lines compared with normal tissues and normal human oral keratinocytes cells. There was a notable positive correlation between SNHG16 and c-Myc expression in OSCC tissues. c-Myc silencing by either shRNA c-Myc or by 10058-F4 (c-Myc inhibitor) resulted in a dose-dependent reduction in SNHG16 levels in CAL-27 and TSCCA cells; conversely, upregulation of c-Myc by pcDNA c-Myc markedly increased SNHG16 expression. Depletion of SNHG16 in CAL-27 cells strikingly inhibited cell proliferation, migration and invasion, as indicated by downregulation of proliferating cell nuclear antigen (PCNA), matrix metalloproteinase (MMP)-2 and MMP-9. Moreover, depletion of SNHG16 induced cell apoptosis and inhibited epithelial-to-mesenchymal transition as indicated by induction of cleaved caspase-3 and epithelial cadherin (E-cadherin) along with reduction of N-cadherin and Snail. Intriguingly, c-Myc knockdown led to the similar functional effects as that of SNHG16 knockdown in TSCCA cells. However, these changes caused by c-Myc knockdown were abrogated by SNHG16 overexpression. Knockdown of SNHG16 conspicuously repressed tumor growth in nude mice. Similarly, silencing of c-Myc markedly inhibited tumor growth and reduced SNHG16 expression in nude mice. Moreover, overexpression of SNHG16 blocked the inhibitory effect of c-Myc silencing on tumor growth in vivo. Thus, we conclude that c-Myc-induced upregulation of SNHG16 enhances progression and carcinogenesis in OSCC.