Esophageal cancer (EC) is a common malignant tumor of the digestive system. Exploring the molecular biological mechanism of EC will help to clarify its carcinogenesis mechanism, find important molecular targets in the process of carcinogenesis, and provide new ideas for the diagnosis and treatment of EC. Phosphatidylinositol-3-kinase (PI3K)/protein kinase B (Akt) signaling pathway is one of the signal transduction pathways most closely related to cell proliferation and apoptosis. The regulation of various downstream molecules affects the proliferation and growth of tumor cells. In this study, we determined the effect of different concentrations of afuresertib on cell viability by MTT assay and determined the effect of afuresertib on cell apoptosis by Annexin V-FITC/PI dual staining. Animal experiments verified the effects of afuresertib on VEGF, bFGF, and PI3K/Akt. Our results indicated that afuresertib is closely related to the survival, proliferation, and apoptosis of esophageal cancer cell lines. More importantly, we found that afuresertib could reduce tumor volume and mass in EC rats through in vivo experiments. In conclusion, afuresertib may exert its antitumor effect by inhibiting the expression of PI3K and Akt-related proteins in rat tumor tissues.

Pancreatic cancer is characterized by poor prognosis and high mortality, while its treatment remains unsatisfactory. Cinchonine, a natural compound present in cinchona bark, is a potential anticancer drug. Whether cinchonine is of relevance to pancreatic cancer therapeutics is unclear. This research showed that the ribosomal RNA‐processing 15 homolog (RRP15) expression is decreased in the pancreatic cancer, and RRP15 knockdown inhibited autophagy, and caused apoptosis in pancreatic cancer cells. Cinchonine treatment inhibits the expression of RRP15 and autophagy, and caused apoptosis by leading to the activation of Nrf2 axis in pancreatic cancer cells. Taken together, the above results indicate that cinchonine treatment inhibited autophagy and induced apoptosis through activating Nrf2 axis by downregulating RRP15 in pancreatic cancer cells.