Currently, there exists an urgent need to investigate the anti-cancer effects of lidocaine on gastric cancer cells. The purpose of the present study was to evaluate the anti-tumor effects and the underlying mechanisms of lidocaine in gastric cancer cells. Our results indicated that lidocaine signifi cantly suppressed proliferation, migration and invasion and induced apoptosis in a dose-dependently manner in human gastric cancer cells. In addition, our data shown that the expression of Bcl-2 was decreased and the level of Bax was increased by lidocaine treatment. Furthermore, we found that lidocaine altered the protein expression of the MAPK pathway. p-p38 was also increased simultaneously, while the level of p38 was not changed. In summary, lidocaine has a prominent anti-tumor activity on gastric cancer cells and is a promising therapeutic agent for the treatment of gastric cancer (Fig. 4, Ref. 32).
ABSTRACT. The aim of this study was to explore methods by which the ERK signaling pathway inhibitor PD98059 (PD) could be used in long-term in vivo experiments. Forty healthy New Zealand rabbits were randomly divided into blank control, model control, PD low-dose, PD high-dose, PD blank, dimethyl sulfoxide (DMSO) control, DMSO blank, and positive control groups. The corresponding treatments were administered to each experimental group over the course of four weeks, after which, total ERK1/2 and ERK5 protein levels, protein phosphorylation, and gene expression were measured in myocardial tissues. Treatment of rabbits with Adriamycin (doxorubicin) resulted in the significant overall differences in ERK1/2 and ERK5 phosphorylation (P < 0.05). Compared with the model control group, changes in phosphorylated ERK1/2 and phosphorylated ERK5 were lowest in the PD high-dose group (P < 0.05). No significant differences in total protein and mRNA levels of myocardial ERK1/2 and ERK5 were detected between the groups after four weeks (P > 0.05). Continuous intravenous injection of PD98059 significantly reduced phosphorylation of ERK1/2 X.Y. Chen et al. 18326©FUNPEC-RP www.funpecrp.com.br Genetics and Molecular Research 14 (4): 18325-18333 (2015) and that of ERK5. In conclusion, Adriamycin-induced myocardiopathy and abnormal ERK signaling might constitute a valuable model foruse in long-term experiments. These methods may provide a theoretical basis for related in vivo studies of long duration.
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