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BackgroundRenal cell carcinoma (RCC) is one of the leading causes of cancer related mortality worldwide. Increasing evidence has shown that microRNAs function as oncogenes or tumor suppressors in human malignancies, but the roles of miR-203 in human RCC is still unclear.MethodsFirst, quantitative real-time PCR (qRT-PCR) was performed to detect miR-203 expression in renal cancer cell lines and clear cell RCC (ccRCC) specimens. Then, the association of miR-203 expression with clinicopathological features and survival was later analyzed. Finally, the roles of miR-203 in regulation of tumor proliferation, migration, invasion, and target gene expression were further investigated.ResultsOur study showed miR-203 was down-regulated in renal cancer cell lines and ccRCC specimens (P < 0.05). Respectively, the low miR-203 expression in ccRCC specimens was associated with advanced clinical features and poorer prognosis (P < 0.05). miR-203 expression was an independent prognostic marker of overall ccRCC patient survival in a multivariate analysis (P < 0.05). Transient forced expression of miR-203 inhibited renal cancer cell growth and metastasis (P < 0.05). In contrast, down-regulation of miR-203 expression promoted renal cancer cell growth and metastasis (P < 0.05). Mechanistic investigations confirmed FGF2 as a direct target of miR-203, and up-regulation of miR-203 could decrease expression of FGF2. Further investigation showed that ectopic expression of FGF2 partially reversed the inhibition effect of enforced miR-203 expression on the malignant phenotypes of renal cancer cells.ConclusionsOur study suggested that miR-203 could be a potential prognostic marker and functions as a tumor suppressor in human renal cancer by post-transcriptionally targeting FGF2.Virtual slidesThe virtual slide(s) for this article can be found here: http://www.diagnosticpathology.diagnomx.eu/vs/6828145701534108.

Objectives: To explore the clinical value of circulating long non-coding RNAs (lncRNAs) as biomarkers to predict fetal congenital heart defects (CHD) in pregnant women. Methods: Differential expression of lncRNAs isolated from the plasma of pregnant women with typical fetal CHD or healthy controls was analyzed by microarray. Gene ontology (GO), pathway and network analysis were performed to study the function of the lncRNAs. Differentially expressed lncRNAs were validated in plasma samples from 62 pregnant women with typical CHD and 62 matched controls by RT-PCR. The sensitivity and specificity of each lncRNA in the diagnosis of fetal CHD was determined by ROC curve analysis. Results: Microarray analysis identified 3694 up-regulated and 3919 down-regulated (fold change ≥2.0) lncRNAs. The top ten significantly differentially expressed, CHD-associated lncRNAs were validated by RT-PCR. Five significantly up-regulated or down-regulated lncRNAs were identified: ENST00000436681, ENST00000422826, AA584040, AA709223 and BX478947 with the AUC of ROC curves calculated as 0.892, 0.817, 0.755, 0.882 and 0.886, respectively. Conclusions: Specific lncRNAs aberrantly expressed in the plasma of pregnant women with typical fetal CHD may play a key role in the development of CHD and may be used as novel biomarkers for prenatal diagnosis of fetal CHD.

Prostate cancer (PCa) is a carcinoma in which fatty acids are abundant. Fatty acid metabolism is rewired during PCa development. Although PCa can be treated with hormone therapy, after prolonged treatment, castration-resistant prostate cancer can develop and can lead to increased mortality. Changes to fatty acid metabolism occur systemically and locally in prostate cancer patients, and understanding these changes may lead to individualized treatments, especially in advanced, castration-resistant prostate cancers. The fatty acid metabolic changes are not merely reflective of oncogenic activity, but in many cases, these represent a critical factor in cancer initiation and development. In this review, we analyzed the literature regarding systemic changes to fatty acid metabolism in PCa patients and how these changes relate to obesity, diet, circulating metabolites, and peri-prostatic adipose tissue. We also analyzed cellular fatty acid metabolism in prostate cancer, including fatty acid uptake, de novo lipogenesis, fatty acid elongation, and oxidation. This review broadens our view of fatty acid switches in PCa and presents potential candidates for PCa treatment and diagnosis.