Downregulation of miR-16 promotes growth and motility by targeting HDGF in non-small cell lung cancer cells

AbstractMicroRNAs play important roles in the development and progression of non-small cell lung cancer (NSCLC). miR-16 functions as a tumor-suppressor and is inhibited in several malignancies. Herein, we validated that miR-16 is downregulated in NSCLC tissue samples and cell lines. Ectopic expression of miR-16 significantly inhibited cell proliferation and colony formation. Moreover, miR-16 suppressed cell migration and invasion in NSCLC cells. Hepatoma-derived growth factor (HDGF) was found to be a direct target of miR-16 in NSCLC cell lines. Rescue experiments showed that the suppressive effect of miR-16 on cell proliferation, colony formation, migration, and invasion is partially mediated by inhibiting HDGF expression. This study indicates that miR-16 might be associated with NSCLC progression, and suggests an essential role for miR-16 in NSCLC

Time resolved scattering relaxation mechanisms of microcavity polaritons

We study the polariton relaxation dynamics for different scattering mechanisms as: Phonon and electron scattering procesess. The relaxation polariton is obtained at very short times by solving the Boltzman equation. Instead of the well-known relaxation process by phonons, we show that the bottleneck effect relaxes to the ground state more efficiently at low pump power intensity when the electron relaxation process is included. In this way, we clearly demonstrate that different relaxation times exist, for which any of these two mechanism is more efficient to relax the polariton population to the ground state.Comment: 10 eps figure

miR-149 Inhibits Non-Small-Cell Lung Cancer Cells EMT by Targeting FOXM1

MicroRNAs (miRNAs) have been implied to play crucial roles for epithelial-to-mesenchymal transition (EMT) of non-small-cell lung cancer cells (NSCLC cells). Here we found that the expression of miR-149, downregulated in lung cancer, was inversely correlated with invasive capability and the EMT phenotype of NSCLC cells. miR-149 inhibited EMT in NSCLC cells. Furthermore, we demonstrated that miR-149 directly targeted Forkhead box M1 (FOXM1), and FOXM1 was involved in the EMT induced by TGF-β1 in A549 cells. Overexpression of FOXM1 restored EMT process inhibited by miR-149. Our work suggested that miR-149 might be an EMT suppressor in NSCLC cells