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Coix lacryma-jobi var. ma-yuen Stapf sprout extract has anti-metastatic activity in colon cancer cells in vitro
- Son, EunSuk, Kim, YoungOck, Park, ChunGeon, Park, KyungHun, Jeong, SungHwan, Park, Jeong-Woong, Kim, Se-Hee
- BMC complementary and alternative medicine 2017 v.17 no.1 pp. 486
- Coix lacryma-jobi, Western blotting, alternative medicine, anaerobic conditions, antineoplastic activity, apoptosis, cell movement, cell proliferation, colorectal neoplasms, crops, deferoxamine, herbal medicines, human umbilical vein endothelial cells, humans, hypoxia, mitogen-activated protein kinase, neoplasm cells, non-specific serine/threonine protein kinase, patients, China
- BACKGROUND: Coix lacryma-jobi var. ma-yuen (Rom.Caill.) Stapf has been used in China as an herbal medicine. Many studies of this plant have reported anti-proliferative and apoptotic activities on human cancer cell lines. Therefore, this study of the anti-metastatic effect of Coix lacryma-jobi var. ma-yuen Stapf sprout extract (CLSE) in colorectal cancer cells may provide a scientific basis for exploring anti-cancer effects of edible crops. METHODS: To evaluate the effect of CLSE on cell proliferation and signaling, we performed a Cell Counting Kit-8 (CCK-8) assay in HCT116 cells and used western blot analysis. Furthermore, scratch-wound healing, transwell migration, matrigel invasion, and adhesion assays were conducted to elucidate the anti-metastatic effects of CLSE under hypoxic conditions in colon cancer cells. RESULTS: First, CLSE decreased deferoxamine (DFO)-induced migration of colon cancer cells by 87%, and blocked colon cancer cell migration by 80% compared with hypoxia control cells. Second, CLSE treatment resulted in a 54% reduction in hypoxia-induced invasiveness of colon cancer cells, and 50% inhibition of adhesive potency through inactivation of the extracellular signal-regulated kinase (ERK) 1/2 and protein kinase b (AKT) pathways. Third, conditioned medium collected from CLSE-treated HCT116 cells suppressed tube formation of human umbilical vein endothelial cells (HUVECs) by 91%. CONCLUSIONS: CLSE inhibited migration, invasion, and adhesion of colon cancer cells and tube formation by HUVECs via repression of the ERK1/2 and AKT pathways under hypoxic conditions. Therefore, CLSE may be used to treat patients with colon cancer.