Inhibition of urethane-induced lung carcinogenesis in mice by a Rhizoma paridis saponin involved EGFR/PI3K/Akt pathway

Lung cancer is one of the most common cancers in the world. Due to a lack of successful treatments for lung cancer, there is a need to evaluate new and effective agents for lung cancer treatment. Rhizoma Paridis saponins (RPS) were deemed effective for the treatment of cancer disease. In the present study, we evaluated the role of RPS on urethane-induced lung carcinogenesis in C57BL/6 mice. As a result, the treatment with RPS reduced the severity of the histopathology on urethane-induced lung tumorigenesis in mice. The mechanisms of its antitumor effect involved in (i) reducing oxidative stress injury through up-regulation of Nrf2 and HO-1, (ii) decreasing the level of inflammatory factors, like COX-2 and PGE2, (iii) activation of caspase-3 through the down-regulation of anti-apoptotic protein (Bcl2) and up-regulation of pro-apoptotic protein (Bax), (iv) decreasing the expression of PCNA, and (v) inhibiting the epidermal growth factor receptor (EGFR)/PI3K/Akt pathway. In conclusion, RPS would be a potent agent inhibiting lung cancer in the future.