D. candidum has in vitro anticancer effects in HCT-116 cancer cells and exerts in vivo anti-metastatic effects in mice

BACKGROUND/OBJECTIVES: D. candidum is a traditional Chinese food or medicine widely used in Asia. There has been little research into the anticancer effects of D. candidum, particularly the effects in colon cancer cells. The aim of this study was to investigate the anticancer effects of D. candidum in vitro and in vivo. MATERIALS/METHODS: The in vitro anti-cancer effects on HCT-116 colon cancer cells and in vivo anti-metastatic effects of DCME (Dendrobium canidum methanolic extract) were examined using the experimental methods of MTT assay, DAPI staining, flow cytometry analysis, RT-PCR, and Western blot analysis. RESULTS: At a concentration of 1.0 mg/mL, DCME inhibited the growth of HCT-116 cells by 84%, which was higher than at concentrations of 0.5 and 0.25 mg/mL. Chromatin condensation and formation of apoptotic bodies were observed in cancer cells cultured with DCME as well. In addition, DCME induced significant apoptosis in cancer cells by upregulation of Bax, caspase 9, and caspase 3, and downregulation of Bcl-2. Expression of genes commonly associated with inflammation, NF-kappaB, iNOS, and COX-2, was significantly downregulated by DCME. DCME also exerted an anti-metastasis effect on cancer cells as demonstrated by decreased expression of MMP genes and increased expression of TIMPs, which was confirmed by the inhibition of induced tumor metastasis in colon 26-M3.1 cells in BALB/c mice. CONCLUSIONS: Our results demonstrated that D. candidum had a potent in vitro anti-cancer effect, induced apoptosis, exhibited anti-inflammatory activities, and exerted in vivo anti-metastatic effects.

Activation of Notch1 Signaling Inhibits Proliferation of Human Colon Carcinoma Cells via Down-regulation of Wnt / 医学研究杂志

Objective To construct the recombinant retroviruses vector PCLNRX-ICN and to explore over-activation Notch1 on the growth of human colon carcinoma cells HT-29.MethodsICN(intracellular domain of Noctch1) genes were inserted into retrovirus expression vector pCLNRX.The expression vector pCLNRX-ICN and packaging vector pCL-10A1 were co-transfected into 293 package cells.The recombinant retroviruses were used to infect HT-29 cells.After being infected,proliferation of HT-29 cells was observed by MTT assay.The expression of c-Myc and ?-catenin detected by RT-PCR and Western Blot.ResultsRecombinant retrovirus vector pCLNRX-ICN was successfully constructed.Overactivation of Notch1 by over-expressing exogenous ICN significantly inhibited the growth of HT-29 cells,and down-regulated ?-catenin,a key regulator of Wnt signaling,in protein level but not in mRNA levels.However,the mRNA or protein levels of c-Myc were not affected by overactivation of Notch1.ConclusionOver-activated Notch1 signaling could inhibit the growth of HT-29 cells partly through down-regulation of Wnt signaling independent of c-Myc inhibition.