PurposeThis study aims to analyze the scientific output of long noncoding RNA (lncRNA) research and construct a model to evaluate publications from the past decade qualitatively and quantitatively.MethodsPublications from 2007 to 2016 were retrieved from the Web of Science Core Collection database. Microsoft Excel 2016 and CiteSpace IV software were used to analyze publication outputs, journals, countries, institutions, authors, citation counts, ESI top papers, H-index, and research frontiers.ResultsA total of 3,008 papers on lncRNA research were identified published by June 17, 2017. The journal, Oncotarget (IF2016, 5.168) ranked first in the number of publications. China had the largest number of publications (1,843), but the United States showed its dominant position in both citation frequency (45,120) and H-index (97). Zhang Y (72 publications) published the most papers, and Guttman M (1,556 citations) had the greatest co-citation counts. The keyword “database” ranked first in research frontiers.ConclusionThe annual number of publications rapidly increased in the past decade. China showed its significant progress in lncRNA research, but the United States was the actual leading country in this field. Many Chinese institutions engaged in lncRNA research but significant collaborations among them were not noted. Guttman M, Mercer TR, Rinn JL, and Gupta RA were identified as good candidates for research collaboration. “Database,” “Xist RNA,” and “Genome-wide association study” should be closely observed in this field.

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Ion-selective electrode (ISE) based potentiometric gas sensors have shown to be promising analytical tools for detection of chemical vapors. However, such sensors are only capable of detecting those vapors which can be converted into ionic species in solution. This paper describes for the first time a polymer membrane ISE based potentiometric sensing system for sensitive and selective determination of neutral vapors in the gas phase. A molecularly imprinted polymer (MIP) is incorporated into the ISE membrane and used as the receptor for selective adsorption of the analyte vapor from the gas phase into the sensing membrane phase. An indicator ion with a structure similar to that of the vapor molecule is employed to indicate the change in the MIP binding sites in the membrane induced by the molecular recognition of the vapor. The toluene vapor is used as a model and benzoic acid is chosen as its indicator. Coupled to an apparatus manifold for preparation of vapor samples, the proposed ISE can be utilized to determine volatile toluene in the gas phase and allows potentiometric detection down to parts per million levels. This work demonstrates the possibility of developing a general sensing principle for detection of neutral vapors using ISEs.

MicroRNAs (miRs) act as important regulators during the development and progression of human cancer; however, the regulatory mechanism of miR-663 in nasopharyngeal carcinoma (NPC) remains unclear. The present study demonstrated that serum miR‑663 levels were significantly increased in patients with NPC compared with healthy controls. In addition, the serum levels of miR‑663 were associated with the grade, lymph node metastasis and clinical stage of NPC. The expression of miR‑663 was increased in NPC C666‑1 cells, compared with normal nasopharyngeal epithelial NP69 cells. The knockdown of miR‑663 markedly decreased the proliferation of C666‑1 cells through the induction of cell cycle arrest at the G1 stage. Cyclin‑dependent kinase inhibitor 2A (CDKN2A) was hypothesized to be a putative target of miR‑663. Further investigation confirmed that miR‑663 was able to directly bind to the 3' untranslated region of CDKN2A mRNA, and to negatively regulate CDKN2A protein expression in C666‑1 cells. Inhibition of CDKN2A expression attenuated the suppressive effects of miR‑663 knockdown on the proliferation and cell cycle progression of C666‑1 cells. In addition, it was observed that the mRNA and protein levels of CDKN2A were decreased in C666‑1 cells compared with NP69 cells. In conclusion, the results of the present study demonstrated that miR‑663 promoted the proliferation and cell cycle progression of NPC cells by directly targeting CDKN2A, suggesting that miR‑663 may become a potential therapeutic target for the treatment of NPC.

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