Cervical cancer is the third most common cancer and the fourth leading cause of malignancy related mortality in women worldwide. CCL19 is highly expressed in human cancer cells, and ligand CCL19 binding to CCR7 induces actin polymerization and pseudopodia formation. However, whether or not CCL19 is involved in EMT of human cervical cancer needs further investigation. Using quantitative PCR and western blot analyses, we found that CCL19 is overexpressed in cervical cancer cell lines and tissues. Knockdown of CCL19 via siRNA inhibited the proliferation of cervical cancer cells by increasing apoptosis. Further analyses showed that inhibitory effects of CCL19 on cell migration and invasion were partly associated with EMT process. In conclusion, these data indicate that CCL19 is abnormally expressed in cervical cancer, indicating a novel and important role for CCL19 in cervical cancer malignant transformation.

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Puerarin, an active ingredient of , has a range of pharmacological effects and excellent pharmacodynamic properties. In the present study, the effect of puerarin on angiotensin II-induced aortic aneurysm formation and the potential underlying molecular mechanisms were examined. The results revealed that puerarin significantly suppressed the viability, and induced the apoptosis, of aneurysm-inducing cells in a time- and dose-dependent manner. Furthermore, treatment with puerarin significantly suppressed the production of reactive oxygen species (ROS) and the expression of matrix metalloproteinase-2 (MMP-2) protein in aneurysm cells. Puerarin treatment significantly increased caspase-9 and -3 activity, induced the protein expression of phosphorylated (p)-Jun and inhibited the protein expression of activator protein 1 (AP-1) in aneurysm cells. It was also demonstrated that Puerarin significantly suppressed the reduced nicotinamide-adenine dinucleotide phosphate (NADPH) oxidase activity in aneurysm cells. Therefore, it was demonstrated that puerarin on suppressed the cell growth of angiotensin II-induced aortic aneurysm formation by affecting the rate of apoptosis, the generation of ROS, MMP-2, AP-1 and p-Jun protein expression and NADPH oxidase.