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Background: Periplocin is a monomeric compound that exhibits anti‐tumor activities. It is extracted from Cortex Periplocae. Objective: This study aimed at determining the effect of periplocin treatment on the apoptosis and proliferation of human pancreatic cancer cells, and to elucidate on its mechanisms of action. Methods: PANC1 and cfpac1 cells were treated with periplocin. Cell proliferation was detected by RTCA, Ki67 immunofluorescence, and a clonogenic assay. The transwell assay was used to examine cell migration and invasion functions. The expression of apoptosis‐associated proteins was detected by flow cytometry and western blotting. Total RNA was extracted from the treated and untreated group of PANC1 cells for RNA‐seq detection and analysis. Differentially expressed genes were screened for GO biological process and KEGG pathway analysis. Finally, CFPAC1 cells were subcutaneously inoculated into BALB / c nude mice to assess tumor growth. Results: Periplocin inhibited the proliferation of PANC1 and CFPAC1 cells and induced their apoptosis by activating the AMPK/mTOR pathway and inhibiting p70 S6K. It also attenuated the cell migration, invasion, and inhibited the growth of cfpac1 xenografts in nude mice. Conclusions: Periplocin inhibits human pancreatic cancer cell proliferation and induces their apoptosis by activating the AMPK / mTOR pathway. [ABSTRACT FROM AUTHOR]

Baohuoside I induces hepatocellular carcinoma apoptosis via targeting mTOR signaling. Baohuoside I inhibits hepatocellular carcinoma proliferation, invasion and migration in vitro and suppresses tumor development in vivo. • Baohuoside I inhibits hepatocellular carcinoma proliferation, invasion and migration. • The inhibition of hepatocellular carcinoma by Baohuoside I is through inducing liver cancer cell apoptosis. • Baohuoside I targeting mTOR signaling to induce liver cancer cell apoptosis. Baohuoside-1 is a flavonoid compound isolated from Epimedium koreanum Nakai. This study tried to systematically explore the potential anti-cancer functions of Baohuoside-1 in Hepatocellular Carcinoma and study related molecular mechanism. Moreover, as a potential candidate anti-cancer agent, Baohuoside-1 has relatively low toxic side effect. Methods: The anti-cancer function including proliferation, invasion and migration of Baohuoside-1 in liver cancer was systematically assessed via colony formation, transwell assay and migration assay. Moreover, the anti-cancer functions of Baohuoside-1 was confirmed based on the nude mouse transplantation tumor experiment. The potential targeted signaling pathway was tested via flow cytometery and western blot analysis. In this study, we present the anti-HCC activity of Baohuoside-1 isolated from Epimedium through examing the effect of Baohuoside-1 on two different human liver cancer cell lines (HuH-7 and HepG2). Baohuoside-1 significantly inhibited the proliferation, invasion and migration of two liver cancer cell lines. Furthermore, the anticancer activity of Baohuoside-1 was confirmed via inhibiting liver tumor growth in nude mice in vivo. Additionally, the influence of Baohuoside-1 on liver cancer apoptosis was examined by analyzing the expression of pro/anti-apoptotic proteins (BAX, Bcl-2, caspase-3, and caspase-8). The potential targeting signaling of Baohuoside-1 was determined via testing key members' expression changes of mTOR and JAK2 signaling. The inhibition of liver cancer by Baohuoside-1 is through targeting mTOR signaling not JAK2 signaling to induce apoptosis. Our study indicates that Baohuoside-1 is a potential candidate drug for therapy against liver cancer. [ABSTRACT FROM AUTHOR]