The human genome holds an extraordinary trove of information about human development, physiology, medicine and evolution. Here we report the results of an international collaboration to produce and make freely available a draft sequence of the human genome. We also present an initial analysis of the data, describing some of the insights that can be gleaned from the sequence.

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Oral mucositis is a common, dose-limiting, acute toxicity of radiation therapy administered for the treatment of cancers of the head and neck. Accumulating data would suggest that the pathogenesis of mucositis is complex and involves the sequential interaction of all cell types of the oral mucosa, as well as a number of cytokines and elements of the oral environment. While a number of studies have reported on gene expression of particular cell types in response to radiation, the overall response of irradiated mucosa has only been evaluated in a limited way. The present study was undertaken to evaluate the expression of a target group of genes using RNA quantification assays and, more broadly, to assess patterns of mucosal gene expression using DNA microarray hybridization. Our results demonstrate the sequential upregulation of a series of genes that, when taken collectively, suggest an intricate functional interaction.

Background To explore the role of non‐coding RNA activated by DNA damage (NORAD), a long non‐coding ribonucleic acid (lncRNA), in non‐small cell lung cancer (NSCLC) and its possible mechanism. Methods Quantitative real‐time polymerase chain reaction was adopted for the detection of the expression levels of NORAD, micro RNA (miR)‐656‐3p, and AKT serine/threonine kinase 1 (AKT1). The effects of NORAD, miR‐656‐3p, and AKT1 on cell proliferation and migration were examined through the Cell Counting Kit‐8 (CCK‐8) and Transwell assay. Subsequently, the binding relationships between miR‐656‐3p and AKT1 and between miR‐656‐3p and NORAD were verified by dual‐luciferase reporter gene assay. Finally, the potential mechanisms of action of NORAD and miR‐656‐3p were explored through the torsion experiment. Results The lncRNA NORAD expression level in NSCLC patients was notably higher than that in people in control group, that in patients with metastasis was higher than that in patients without metastasis, and that in patients with NSCLC in stage III‐IV was significantly higher than that in patients with NSCLC in stage I‐II. Elevation of NORAD stimulated the proliferation and migration of NSCLC A549/H460 cells. According to the reporter gene assay, NORAD could bind to miR‐656‐3p. Besides, miR‐656‐3p was significantly under‐expressed in cancer tissues of patients with NSCLC, and overexpression of miR‐656‐3p could block the proliferation and migration of A549/H460 cells and reversed promotion on cell proliferation and migration by NORAD. Furthermore, the reporter gene assay revealed that the overexpression of AKT1, a miR‐656‐3p target gene, could reverse miR‐656‐3p's inhibitory effect on the proliferation and migration of A549/H460 cells. Conclusion LncRNA NORAD is capable of promoting the proliferation and migration of NSCLC cells, and its mechanism may be that it increases the AKT1 expression by adsorbing miR‐656‐3p.