Knockdown or low expression of these lncRNAs led to decreased expression of their neighboring proteincoding genes, including several master regulators of cellular differentiation. Our microarray displayed a portion of enhancerlike lncRNAs. Like classical enhancers, lncRNAs are orientation independent and require a minimal promoter in their target genes to enhance their transcriptions. Although the precise molecular mechanism is yet to be defined, this group of lncRNAs illustrates that eukaryotic transcription is very tightly regulated by overlapping mechanisms. All of the examples described indicate that lncRNAs can serve as a portion markers of active regulatory pathways. More about this, the lncRNAs researched here should be distinguished from transcripts that are produced at enhancer sites, the function of which has yet to be determined. We also identified the differentially expressed lncRNAs and nearby coding gene pairs. It was reported that knockdown or low expression of certain lncRNAs can led to decreased expression of their neighboring protein-coding genes, including several master regulators of cellular differentiation and that lncRNAs and nearby coding genes may represent shared upstream regulation or local transcriptional effects. Thus, the subgroup analysis of lncRNAs may help us to explore the relationship between lncRNAs and RCCC. Most of the lncRNAs have a distinct spatial and temporal specificity in the process of organismal differentiation and development. One study for 1300 lncRNAs of mice illustrated that in different parts of the brain tissue, lncRNAs have different expression patterns and lncRNAs expression signatures have been described in prostate carcinoma, hepatic tumor. Then in the development of RCCC, there may be different expression patterns of lncRNAs and the differentially expressed lncRNAs may execute special cellular function in RCCC. One previous study have shown the antitumor DNA topoisomerase I inhibitor camptothecin increases the cellular levels of two antisense lncRNAs at the 59 and 39 ends of the human HIF-1a gene, they also proved the two antisense lncRNAs at the 59 and 39 that induced nuclear membrane trafficking and response to partially different kinds of stress expressed in human kidney cancer tissues. To the best of our knowledge, this is the first study that describes the expression profiles of human lncRNAs in RCCC by microarray, a collection of deregulated lncRNAs were aberrantly expressed in RCCC compared to matched NT sample groups. Probably, these deregulated lncRNAs play a key or partial role as oncogenes or tumor suppressors in the development and/or progression of this carcinoma. More work will be needed to determine whether these lncRNAs can serve as new therapeutic targets and diagnostic biomarkers in RCCC. The risk for progression of renal function is contributed to traditional risk factors such as hypertension, diabetes, and dyslipidemia and non-traditional risk factors including cardiovascular disease. Progressive decline in renal function was significantly associated with high cardiovascular morbidity and mortality, independent of baseline renal function. Therefore, identifying the patients with rapid renal function progression for aggressive treatment interventions is important in disease attenuation and prolonged survival. Recently, echocardiographic measures of left ventricular function and structure as well as left INCB28060 atrial size have been reported to predict adverse renal outcomes.