Establishment of a visualized mouse orthotopic xenograft model of nasopharyngeal carcinoma.

Mouse orthotopic xenograft tumor models are commonly employed in studies investigating the mechanisms underlying the development and progression of tumors and their preclinical treatment. However, the unavailability of mature and visualized orthotopic xenograft models of nasopharyngeal carcinoma limits the development of treatment strategies for this cancer. The aim of this study was to provide a simple and reliable method for building an orthotopic xenograft model of nasopharyngeal carcinoma. Human nasopharyngeal carcinoma (C666-1-luc) cells, stably expressing the firefly luciferase gene, were injected subcutaneously into the right axilla of BALB/C nude mice. Four weeks later, the resulting subcutaneous tumors were cut into small blocks and grafted into the nasopharynx of immunodeficient BALB/C nude mice to induce tumor formation. Tumor growth was monitored by bioluminescence imaging and small animal magnetic resonance imaging (MRI). The expression of histological and immunological antigens associated with orthotopic xenograft nasopharyngeal carcinoma was analyzed by tissue section analysis and immunohistochemistry (IHC). A visualized orthotopic xenograft nasopharyngeal carcinoma model was successfully developed in this study. Luminescence signal detection, micro-MRI, and hematoxylin and eosin staining revealed the successful growth of tumors in the nasopharynx of the nude mice. Moreover, IHC analysis detected cytokeratin (CK), CK5/6, P40, and P63 expression in the orthotopic tumors, consistent with the reported expression of these antigens in human nasopharyngeal tumors. This study established a reproducible, visual, and less lethal orthotopic xenograft model of nasopharyngeal carcinoma, providing a platform for preclinical research.

Ozone decomposition on transition-metal-atom anchored graphdiyne: Insights from computation and experiment.

Transition-metal-atom anchored graphdiynes (TM@GDY, TM = Mn, Fe, Co, Ni and Cu) have already been synthesized and found applications in hydrogen evolution, nitrogen fixation and etc. By means of first-principle predictions and test experiments, we propose here that Fe@GDY and Co@GDY are efficient catalysts for the sustainable conversion of O3 to O2. These two catalysts can spontaneously chemisorb O3 with zero reaction barrier and have low O3 conversion barriers (0.31 eV and 0.19 eV, respectively). The O3 decomposition experiment in a continuous flow membrane reactor and electron paramagnetic resonance results verify that Fe@GDY and Co@GDY are efficient catalysts under humid conditions. Raman spectra prove the formation of the key Fe-O/Co-O and FeOO and CoOO intermediates. The hydrophobic nature of graphdiyne and the strongest chemisorption of O3 among tested ambient gases, make Fe@GDY and Co@GDY ideal catalysts under both dry and humid conditions. These findings would stimulate future explorations on metal anchored GDY-based catalysts for applications of toxic gas decomposition or fixation.

Long Non-Coding RNA LINC01572 Promotes Hepatocellular Carcinoma Progression via Sponging miR-195-5p to Enhance PFKFB4-Mediated Glycolysis and PI3K/AKT Activation.

Background: Accumulating evidence indicates that type 2 diabetes mellitus (T2DM) is a risk factor for hepatocellular carcinoma (HCC), and T2DM-associated HCC represents a common type of HCC cases. We herein identify an lncRNA LINC01572 that was aberrantly upregulated in T2DM-related HCC via high-throughput screening. Based on this, the study was undertaken to identify the functional role and mechanism of LINC01572 in HCC progression. Methods: RT-qPCR was used to detect the expressions of LINC01572 in HCC tissues and cell lines. Gain- or loss-of-function assays were applied to evaluate the in vitro and in vivo functional significance of LINC01572 in the HCC cell proliferation, migration, and invasion using corresponding experiments. Bioinformatics, RIP, RNA pull-down, and luciferase reporter assays were performed to explore the regulatory relationship of the LINC01572/miR-195-5p/PFKFB4 signaling axis. Result: In this study, we profiled lncRNAs in HCC tissues and corresponding adjacent tissues from HCC patients with T2DM by RNA sequencing. Our data showed that LINC01572 was aberrantly upregulated in HCC tissues as compared with control, especially in those with concurrent T2DM. The high level of LINC01572 was correlated with advanced tumor stage, increased blood HbA1c level, and shortened survival time. The overexpression of LINC01572 significantly promoted HCC cell proliferation, migration, invasion, and epithelial-to-mesenchymal transition (EMT), while the knockdown of LINC01572 had the opposite effects on HCC cells. A mechanistic study revealed that LINC01572-regulated HCC progression via sponging miR-195-5p to increase the level of PFKFB4 and subsequent enhancement of glycolysis and activation of PI3K-AKT signaling. Conclusion: LINC01572 acts as ceRNA of miR-195-5p to restrict its inhibition of PFKFB4, thereby enhancing glycolysis and activates PI3K/AKT signaling to trigger HCC malignancy.