Semiconductor Polymer Dots Induce Proliferation in Human Gastric Mucosal and Adenocarcinoma Cells

Abstract

We investigated the cellular uptake behavior and cell viability of semiconducting polymer dots (Pdots) on human gastric adenocarcinoma (SGC-7901) cells and human gastric mucosal (GES-1) cells. MTT studies indicate the Pdot treatment induces obvious cell proliferation in both types of cell lines. We performed further investigations such as reactive oxygen species (ROS) generation and mitochondrial membrane potential (MMP) change, which indicate that the cell proliferation is in good agreement with the increase in the ROS and MMP levels. Moreover, expression of protein kinase B (Akt) decreased as the Pdot concentration increases, but the expression of protein dual-phosphorylated Erk (p-Erk) and phosphorylated c-Jun N-terminal kinases (p-JNK) were increased. These effects indicated that the Pdots could promote the growth of SGC-7901 cells and GES-1 cells by appropriately regulating the expressions of protein Akt, p-Erk, and p-JNK.