Upregulation of miR-370 contributes to the progression of gastric carcinoma via suppression of FOXO1.

FOXO1 is downregulated in a number of cancers. However, the underlying mechanisms are poorly understood. In this study, we report that the expression of miR-370 was upregulated in gastric cancer cell lines and gastric cancer tissues. Overexpression of miR-370 in gastric cancer cells promoted the cell proliferation and anchorage-independent growth, while silencing of miR-370 showed opposite effects. miR-370-induced proliferation was correlated with the downregulation of cyclin-dependent kinase inhibitors, p27(Kip1) and p21(Cip1), and the upregulation of the cell cycle regulator cyclin D1. Furthermore, we identified that FOXO1 is the functional target of miR-370. Restored expression of FOXO1 together with miR-370 strongly abrogated miR-370-induced cell proliferation. Taken together, our results revealed a novel mechanism of FOXO1 suppression mediated by miR-370 in gastric cancer.

Propofol reduces MMPs expression by inhibiting NF-κB activity in human MDA-MB-231 cells.

Propofol is a common clinical anesthesia agent which is now widely used in relieving pain of patients with chronic cancer as an adjuvant therapy. In our study, we found another effect of propofol in the therapy of chronic cancer patients. We used the breast cancer cell lines to detect the effects and molecular mechanisms of clinically relevant concentrations of propofol, finding that propofol reduced the level of MMP breast cancer by inhibition of NF-κB pathways, which restrained migration and invasion of breast cancer cells significantly. Our finding provides a new sight into propofol in cancer treatment and, suggesting that propofol not only can be an anesthesia agent which reduces pain but plays a important role of inhibiting the invasion and migration of breast cancer cells in the therapy of chronic breast cancer patients.