No abstract

The aim of this study was to explore the association of specific microRNAs (miRNAs) with the development of esophageal cancer (EC) and to identify new molecular markers for EC by analyzing the expression profiles of miRNAs in EC tissues. The expression profiles of miRNAs in paired EC and paracancerous normal tissues were detected and bioinformatically analyzed using miRNA assays. The outcomes were validated using real-time polymerase chain reaction. The miRNA assays revealed a total of 60 differentially expressed miRNAs in the EC tissues compared with those in the paracancerous normal tissues. Among them, 51 had doubled or more than doubled their expression levels and 9 had halved their expression levels. The most markedly upregulated miRNAs were hsa-miR-15a, hsa-miR-28-3p, hsa-miR-31, hsa-miR-99b, hsa-miR-101, hsa-miR-130a, hsa-miR-143, hsa-miR-196b, hsa-miR-200a, hsa-miR-210, hsa-miR-452 and hsa-miR-27a, whereas the most markedly downregulated miRNAs included hsa-miR-30b, hsa-miR-223, hsa-miR-454, hsa-miR-486, hsa-miR-574-3p and hsa-miR-126. Specific miRNA expression profiles exist in EC tissues and may serve as novel EC molecular markers.

Proper temporal and spatial activation of stem cells relies on highly coordinated cell signaling. The primary cilium is the sensory organelle that is responsible for transmitting extracellular signals into a cell. Primary cilium size, architecture, and assembly–disassembly dynamics are under rigid cell cycle‐dependent control. Using mouse incisor tooth epithelia as a model, we show that ciliary dynamics in stem cells require the proper functions of a cholesterol‐binding membrane glycoprotein, Prominin‐1 (Prom1/CD133), which controls sequential recruitment of ciliary membrane components, histone deacetylase, and transcription factors. Nuclear translocation of Prom1 and these molecules is particularly evident in transit amplifying cells, the immediate derivatives of stem cells. The absence of Prom1 impairs ciliary dynamics and abolishes the growth stimulation effects of sonic hedgehog (SHH) treatment, resulting in the disruption of stem cell quiescence maintenance and activation. We propose that Prom1 is a key regulator ensuring appropriate response of stem cells to extracellular signals, with important implications for development, regeneration, and diseases.