Scoparone inhibits pancreatic cancer through PI3K/Akt signaling pathway
Na Li, Fan Yang, Dong-Yan Liu, Jintao Guo, Nan Ge, Siyu Sun
Abstract
BACKGROUND: Pancreatic cancer is a highly malignant tumor of the gastrointestinal system whose emerging resistance to chemotherapy has necessitated the development of novel antitumor treatments. Scoparone, a traditional Chinese medicine monomer with a wide range of pharmacological properties, has attracted considerable attention for its antitumor activity. AIM: To explore the potential antitumor effect of scoparone on pancreatic cancer and the possible molecular mechanism of action. METHODS: effect of scoparone on pancreatic cancer cell proliferation was detected using a xenograft tumor model in nude mice as well as immunohistochemistry. RESULTS: values of 225.2 μmol/L and 209.1 μmol/L, respectively. Wound healing and transwell assays showed that scoparone inhibited the migration and invasion of pancreatic cancer cells. Additionally, flow cytometry confirmed that scoparone caused cell cycle arrest and induced apoptosis. Scoparone also increased the expression levels of Bax and cleaved caspase-3, decreased the levels of MMP9 and Bcl-2, and suppressed the phosphorylation of Akt without affecting total PI3K and Akt. Moreover, compared with the control group, xenograft tumors, in the 200 μmol/L scoparone treatment group, were smaller in volume and lighter in weight, and the percentages of Ki65- and PCNA-positive cells were decreased. CONCLUSION: through the PI3K/Akt signaling pathway.