Dexmedetomidine represses proliferation and promotes apoptosis of esophageal cancer cells by regulating C-Myc gene expression via the ERK signaling pathway.

OBJECTIVE: The aim of this study was to investigate the effects of dexmedetomidine (DEX) on proliferation and apoptosis of esophageal cancer (EC) cells, and to explore the possible underlying mechanism. MATERIALS AND METHODS: EC cells (Eca109) were randomly divided into two groups, namely, Control group and DEX group. The viability, proliferation, and apoptosis of Eca109 cells were detected using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, 5-Ethynyl-2'-deoxyuridine (EdU) staining and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) staining, respectively. Meanwhile, the messenger ribonucleic acid (mRNA) and protein expression levels of extracellular signal-regulated kinase (ERK) 1/2 and c-Myc in Eca109 cells were measured by quantitative Reverse Transcription-Polymerase Chain Reaction (qRT-PCR) and Western blotting, respectively. RESULTS: The viability of Eca109 cells was remarkably weakened in DEX group when compared with Control group (p<0.05). DEX could significantly inhibit the proliferation and promote the apoptosis of Eca109 cells (p<0.05). Moreover, the mRNA and protein levels of ERK1/2 and c-Myc in Eca109 cells declined notably (p<0.05). CONCLUSIONS: DEX represses the proliferation and facilitates the apoptosis of Eca109 cells prominently. The possible underlying mechanism may be associated with the inhibition of c-Myc gene expression through the ERK signaling pathway.

Role of visfatin in promoting proliferation and invasion of colorectal cancer cells by downregulating SDF-1/CXCR4-mediated miR-140-3p expression.

OBJECTIVE: Visfatin is significantly upregulated in colorectal cancer (CRC). However, its exact role in CRC progression and the regulatory mechanism involved in this process have not been fully illuminated. The aim of this study was to investigate the roles of visfatin in CRC progression and the potential molecular mechanism. MATERIALS AND METHODS: In vitro, two CRC cell lines (DLD-1 and SW480) were transfected with visfatin, si-visfatin, and their control vectors. Some cells were transfected with miR-140-3p mimics or miRNA negative control. Cell Counting Kit-8 and transwell invasive assays were used to detect cell proliferation and invasion ability. Luciferase reporter assays were performed to confirm whether CXC motif chemokine receptor 4 (CXCR4) directly targets miR-140-3p. Western blotting and qRT-PCR analyses were respectively conducted to evaluate the protein and mRNA levels of stromal cell-derived factor-1 (SDF-1) and CXCR4. In vivo, DLD-1 cells transfected with visfatin construct or vector control were inoculated into nude mice. After 5 weeks, the mice were sacrificed, and the tumor nodules were weighed. The expression of visfatin, SDF-1, and CXCR4 in tumor tissues was detected via immunohistochemistry analysis. RESULTS: In vitro, the transfection of visfatin promoted the proliferation and invasion of CRC cells, as well as upregulated the expression of SDF-1/CXCR4. MiR-140-3p directly targets the 3'untranslated region of CXCR4. MiR-140-3p expression was downregulated by treatment with visfatin, and miR-140-3p exerted similar effects to those of visfatin knockdown on the proliferation and invasion of CRC cells. In vivo, visfatin stimulated CRC tumor growth and downregulated miR-140-3p expression, whereas it upregulated SDF-1/CXCR4 expression. CONCLUSIONS: Visfatin promotes CRC progression by downregulating the SDF-1/CXCR4-mediated expression of miR-140-3p both in vitro and in vivo.

Fast resistive reconnection regime in the nonlinear evolution of double tearing modes.

Phases of nonlinear double tearing modes are studied numerically. The first two phases lead to the formation and growth of magnetic islands and are followed by a fast reconnection phase to complete the process, driven by a process of neighboring magnetic separatrices merging and magnetic islands coupling. The fast growth can be understood as a result of the island interaction equivalent to a steadily inward flux boundary driven. Resistivity dependences for various phases are studied and shown by scaling analysis for the first time. It is found that after an early Sweet-Parker phase with a eta(1/2)-scale, a slow nonlinear phase in a Rutherford regime with a eta(1)-scale is followed by the fast reconnection phase with a eta(1/5)-scale.