Yan Gao

LncRNA TUG1, a tumor oncogene associated with various human cancers, has been reported to be involved in regulating various cellular processes, such as proliferation, apoptosis and invasion through targeting multiple genes. However, its biological function in thyroid cancer cells has not been elucidated. The aim of this study is to measure TUG1 expression level and evaluate its function in thyroid cancer cells. LncRNA TUG1 expression levels in thyroid cancer tissues and three thyroid cancer cell lines (the ATC cell lines SW1736 and KAT18 and the FTC cell line FTC133) were assessed by qRT-PCR and compared with that of the human normal breast epithelial cell HGC-27. MTT assay, colony formation assay, transwell assay and western blot analysis were performed to assess the effects of TUG1 on proliferation, metastasis and EMT formation in thyroid cancer cells in vitro. Rescue assay was performed to further confirm that TUG1 contributes to the progression of thyroid cancer cells through regulating miR-145/ZEB1 signal pathway. LncRNA TUG1 was found to be up-regulated in thyroid cancer tissues and thyroid cancer cells compared with that in the human normal breast epithelial cell HGC-27. Increased lncRNA TUG1 expression was found to significantly promote tumor cell proliferation, and facilitate cell invasion, while down-regulated TUG1 could obviously inhibit cell proliferation, migration/invasion and reverse EMT to MET. These results indicated that TUG1 may contribute to the progression of thyroid cancer cells by function as a ceRNA competitive sponging miR-145, and that lncRNA TUG1 is associated with tumor progression in thyroid cancer cells.

Metal-organic frameworks (MOFs) are a new variety of solid crystalline porous functional materials. As an extension of inorganic porous materials, it has made important progress in preparation and application. MOFs are widely used in various fields such as gas adsorption storage, drug delivery, sensing, and biological imaging due to their high specific surface area, porosity, adjustable pore size, abundant active sites, and functional modification by introducing groups. In this paper, the types of MOFs are classified, and the synthesis methods and functional modification mechanisms of MOFs materials are summarized. Finally, the application prospects and challenges of metal-organic framework materials in the biomedical field are discussed, hoping to promote their application in multidisciplinary fields.

// Zhijun Pei 1, * , Xian Du 2, * , Yafeng Song 1 , Lin Fan 3 , Fuyan Li 1 , Yan Gao 1 , Ruimin Wu 1 , Yijia Chen 1 , Wei Li 1 , Hong Zhou 1 , Yi Yang 1 , Jing Zeng 4 1 Department of PET Center & Institute of Anesthesiology and Pain, Taihe Hospital, Hubei University of Medicine, Shiyan, Hubei Province, 442000, China 2 Department of General Surgery II, Taihe Hospital, Hubei University of Medicine, Shiyan, Hubei Province, 442000, China 3 Department of Ophthalmology, Taihe Hospital, Hubei University of Medicine, Shiyan, Hubei Province, 442000, China 4 Department of Infection Control, Taihe Hospital, Hubei University of Medicine, Shiyan, Hubei Province, 442000, China * These authors have contributed equally to this work Correspondence to: Jing Zeng, email: zengjingphd@163.com Keywords: bladder cancer, CASC2, Wnt/β-catenin, proliferation, metastasis Received: December 27, 2016     Accepted: January 17, 2017     Published: February 09, 2017 ABSTRACT Long noncoding RNAs cancer susceptibility candidate 2 (CASC2) have been demonstrated as playing crucial regulatory roles in a few of cancers. However, the biological function of lncRNA CASC2 in bladder cancer are still unclear. In this study, we found that lncRNA CASC2 was significantly down-regulated in bladder cancer tissues and cell lines by quantitative real time-PCR and associated with advanced TNM stage (III/IV). Moreover, overexpression of lncRNA CASC2 remarkably reduced the cell growth, migration and invasion, as well as promoted early apoptosis of bladder cancer cell in vitro . Furthermore, we illustrated that lncRNA CASC2 inhibited Wnt/β-catenin signal pathway activity by decrasing the β-catenin expression and reversing the downstream target gene expression of Wnt signaling pathway. Taken together, lncRNA CASC2 plays an pivotal role in bladder tumorigenesis and progression and may act as a potential biomarker for the treatment of bladder cancer.

The great preclinical promise of the pancreatic endoplasmic reticulum kinase (PERK) inhibitors in neurodegenerative disorders and cancers is marred by pancreatic injury and diabetic syndrome observed in PERK knockout mice and humans lacking PERK function and suffering from Wolcott-Rallison syndrome. PERK mediates many of the unfolded protein response (UPR)-induced events, including degradation of the type 1 interferon (IFN) receptor IFNAR1 in vitro. Here we report that whole-body or pancreas-specific Perk ablation in mice leads to an increase in IFNAR1 protein levels and signaling in pancreatic tissues. Concurrent IFNAR1 deletion attenuated the loss of PERK-deficient exocrine and endocrine pancreatic tissues and prevented the development of diabetes. Experiments using pancreas-specific Perk knockouts, bone marrow transplantation, and cultured pancreatic islets demonstrated that stabilization of IFNAR1 and the ensuing increased IFN signaling in pancreatic tissues represents a major driver of injury triggered by Perk loss. Neutralization of IFNAR1 prevented pancreatic toxicity of PERK inhibitor, indicating that blocking the IFN pathway can mitigate human genetic disorders associated with PERK deficiency and help the clinical use of PERK inhibitors.