Baicalin suppresses lung carcinoma and lung metastasis by SOD mimic and HIF-1α inhibition

The dose-related toxicity of anticancer drugs in chemotherapy of clinical carcinoma is the major obstacle to prolonged survival, we want to investigate selective therapeutic efficacy of baicalin on lung carcinoma and explain the basis underlying this phenomenon. In vitro, baicalin inhibited cell proliferation of human lung carcinoma A549 and mouse lewis lung cancer (LLC) in a dose- and time-dependent manner. The inhibitory activity of baicalin against cancer cells was promoted by superoxide dismutase (SOD) addition or hypoxia-inducible factor-1alpha (HIF-1α) knockdown and was reduced by SOD knockdown but not hypoxia. In vivo, baicalin suppressed tumor growth and prolonged survival in C57BL/6 mice bearing LLC tumor and nude mice bearing A549 carcinoma without systemic toxicity. Further studies showed that baicalin inhibited HIF-1α and enhanced SOD activity without affecting catalase and glutathione-S-transferase (GST) in cancer cells. In addition, baicalin also exhibited a superoxide anion scavenging activity. In conclusion, baicalin could selectively suppress lung carcinoma and lung metastasis by SOD mimic and HIF-1α inhibition.