Cyclin A2 regulates symmetrical mitotic spindle formation and centrosome amplification in human colon cancer cells.

Colon cancer is one of the most fatal cancers in the United States, and is characterized by the presence of chromosomal instability (CIN), causes of which are largely unclear. Emerging evidence indicates that abnormal spindle geometry and supernumerary centrosomes lead to CIN in cells. However, if and how spindle geometry defects and centrosomes amplification occur in colon cancer remains unknown.

MiR-211 inhibits cell epithelial-mesenchymal transition by targeting MMP9 in gastric cancer.

Recent studies have demonstrated that the dysregulation of miRNAs are frequently associated with cancer progression including gastric cancer (GC). MiR-211 was found to act as tumor suppressor in GC, however, the functional role of miR-211 involved in GC cell epithelial-mesenchymal transition (EMT) process still to be investigated. In the study, we demonstrated that miR-211 was lower expression in gastric cancer tissues compared with adjacent normal tissues.

Deletion of Slc26a6 alters the stoichiometry of apical Cl-/HCO-3 exchange in mouse pancreatic duct.

To define the stoichiometry and molecular identity of the Cl(-)/HCO(3)(-) exchanger in the apical membrane of pancreatic duct cells, changes in luminal pH and volume were measured simultaneously in interlobular pancreatic ducts isolated from wild-type and Slc26a6-null mice. Transepithelial fluxes of HCO(3)(-) and Cl(-) were measured in the presence of anion gradients favoring rapid exchange of intracellular HCO(3)(-) with luminal Cl(-) in cAMP-stimulated ducts. The flux ratio of Cl(-) absorption/HCO(3)(-) secretion was ∼0.