Long non-coding RNAs (lncRNAs) have a critical role in cancer initiation and progression, and thus may mediate oncogenic or tumor suppressing effects, as well as be a new class of cancer therapeutic targets. We performed high-throughput sequencing of RNA (RNA-seq) to investigate the expression level of lncRNAs and protein-coding genes in 30 esophageal samples, comprised of 15 esophageal squamous cell carcinoma (ESCC) samples and their 15 paired non-tumor tissues. We further developed an integrative bioinformatics method, denoted URW-LPE, to identify key functional lncRNAs that regulate expression of downstream protein-coding genes in ESCC. A number of known onco-lncRNA and many putative novel ones were effectively identified by URW-LPE. Importantly, we identified lncRNA625 as a novel regulator of ESCC cell proliferation, invasion and migration. ESCC patients with high lncRNA625 expression had significantly shorter survival time than those with low expression. LncRNA625 also showed specific prognostic value for patients with metastatic ESCC. Finally, we identified E1A-binding protein p300 (EP300) as a downstream executor of lncRNA625-induced transcriptional responses. These findings establish a catalog of novel cancer-associated functional lncRNAs, which will promote our understanding of lncRNA-mediated regulation in this malignancy.

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The O K-edge x-ray absorption near-edge-structure (XANES) spectra of UO2 and CeO2 are presented and interpreted. Using different-size clusters around the excited atom in the full multiple-scattering (MS) simulation, we are able to link the features present in the spectra of each oxide to its specific atomic arrangement and electronic structure. The structures at the edge originate from oxygen 2p states hybridized with f and d orbitals of the cation split by the cubic crystal field. All of the other features come from MS with the neighbouring shells of the central oxygen atoms.

Phenotypic modulation from a contractile to a proliferative state within vascular smooth muscle cells has a critical role in the pathogenesis of a variety of cardiovascular diseases. To investigate the characterization of corpus cavernosum smooth muscle cell phenotype in diabetic rats with erectile dysfunction, a group of Sprague--Dawley rats (n ¼ 30) were induced by intraperitoneal injection of streptozotocin (60 mg kg À1 ) and screened by subcutaneous injection of apomorphine (100 mg kg À1 ) for the measurement and comparison of the penile erections, and then three different groups were defined. Primary corpus cavernosum smooth muscle cells were cultured and passaged. The cavernous tissue segments were subjected to quantitative real-time polymerase chain reaction to determine the expressions of smooth muscle a-actin (SMA), SM myosin heavy chain (SMMHC), smoothelin, calponin and myocardin. Cell contractility in vitro and western blot analysis of SMA and SMMHC in the cavernous tissues and cells were determined. Compared with the control group (n ¼ 8) and the diabetes mellitus group (n ¼ 5), the expressions of SMA, calponin, SMMHC, smoothelin and myocardin mRNA were decreased in the cavernous tissues in rats of the diabetic erectile dysfunction group (n ¼ 15; P ¼ 0.001 and 0.02, P ¼ 0.014 and 0.012, both Po0.001, P ¼ 0.005 and o0.001, P ¼ 0.003 and 0.035, respectively). The levels of SMA and SMMHC proteins showed a significant decrease in cavernous tissues and cultured cells in rats of the diabetic erectile dysfunction group. Cells of the diabetic erectile dysfunction group exhibited significantly less contractility compared with those of other groups (Po0.001). Corpus cavernosum SM cell possesses the ability to modulate the phenotype under hyperglycemic conditions, which could have a key role in the pathogenesis of diabetic erectile dysfunction. Keywords: diabetes mellitus; erectile dysfunction; smooth muscle INTRODUCTION Erectile dysfunction (ED), a distressing complication of diabetes mellitus (DM), 1 is three times more common in diabetic male rats than in non-diabetic male rats. It has been reported that about 35--90% of diabetic male rats suffer from ED. 2,3 The pathogenesis of DM-related ED may be involved in many aspects; however, it was well known that vascular causative factors contribute significantly. 4 Corpus cavernosum smooth muscle (CCSM), the structural basis of cavernous space relaxing and penile erection, has a key role in the change of hemodynamics during penile erection. CCSM cell relaxation mediated by parasympathetic neurotransmission, nitric oxide, electrophysiological events and possibly other regulatory factors is necessary for normal penile erection. 5 It has been observed that the CCSM cell mass was lost in diabetic rats with ED, and the remaining SM cells were unable to achieve sufficient relaxation to attain the high intracorporeal pressures that are necessary for the passive occlusion of the veins that egress the corporal bodies as they traverse underneath and through the tunica albu...