Litchi (Litchi chinensisSonnnerat, Sapindaceae), known as Chinese Cherry, is a subtropical fruit tree originating from southern China. Litchi seed extracts have diverse pharmacological effects, including anticancer. However, its anticancer effects and mechanisms on prostate cancer have not been determined. In this study, we used n-butyl alcohol extract of Litchi seed (NLS) to treat prostate cancer PC3, DU145, RM1 and C4-2B cells. NLS induced a significant decrease in cell viability and clonogenic growth in a dose-dependent manner. NLS induced cell apoptosis and cell cycle G1/S phase arrest by inactivating Akt signaling pathway, which were associated with activation of mitochondrial caspase-dependent apoptotic cascades, up-regulation of cyclin-dependent kinase (CDK) inhibitors p21 and p27, and inhibition of correlated cyclin/CDK network. In addition, NLS treatment significantly decreased cell migration and invasion via phenotypic inversion of EMT, correlated with increased expression of E-cadherin and β-catenin, and decreased expression of vimentin and snail, which is partially attributed to inhibiting Akt/GSK-3β signaling pathway. Finally, PC3 xenograft nude mice treated with NLS in vivo showed a significant decrease in tumor size without toxicity. These findings suggest that NLS has potential for development into a safe and potent alternative therapy for prostate cancer patients.

Our findings reveal that ASA inhibits the proliferation and promotes apoptosis in the human colon cancer cell line SW480. Down-regulation of Bcl2 expression might represent a potential mechanism by which ASA induces apoptosis in this COX-2 negative colon cancer cell line. Our results also suggest that ASA decreases the invasive potential of these colon cancer cells. Decreased CEA content and CD44v6 expression and elevated nm23 expression may contribute to the effect of ASA on invasive potential of SW480 colon cancer cells.

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Background Oridonin has been shown to exhibit potent anti-tumor activity, but the exact mechanisms underlying this activity remains unclear. Here, we investigated whether oridonin could synergistically enhance the activity of gemcitabine against BxPC-3 pancreatic cancer cells. Methods CCK-8 assays were conducted to determine cell viability. The cellular morphology was observed under light microscope and compared with normal cell. Apoptotic cells were quantified by flow cytometry. RT-PCR, Western blot analysis and immunohistochemical methods were employed to analyze related-gene and protein expression. A xenograft tumor model was conducted whereby BxPC-3 cells were introduced into nude mice to detect anti-tumor effects in vivo . Results In vitro , oridonin inhibited the proliferation of BxPC-3 and Panc-1 cells cells in a concentration and time dependent manner. In addition, oridonin dose-dependently induced Panc-1 cellular morphology changes. Besides, In BxPC-3 cells oridonin potentiated gemcitabine-induced apoptosis. oridonin induced Bax translocation from cytosolic to mitochondrial compartments. This was accompanied by the release of the apoptogenic protein Smac and inhibition of its downstream target XIAP. These effects were further enhanced by combined treatment with oridonin and gemcitabine. In vivo , both oridonin alone and in combination with gemcitabine significantly suppressed tumor growth in a Bax- and Smac-dependent manner. Conclusions Oridonin can potentiate the effects of gemcitabine through Bax- and Smac-dependent mitochondrial signaling pathways in BxPC-3 pancreatic cancer cells. Therefore, oridonin has the potential to be used clinically in the treatment of pancreatic cancer.