Erianin regulates epithelial-mesenchymal transformation and angiogenesis of colorectal cancer HT29 cells via the Hedgehog signal pathway
Article
Figures
Metrics
Preview PDF
Reference
Related
Cited by
Materials
Abstract:
Objective: To investigate the mechanism of the inhibitory effects of dendrobium etract erianin (ER) on epithelial-mesenchymal transition (EMT) and angiogenesis of colorectal cancer HT29 cells based on the Hedgehog signal pathway. Methods: HT29 cells were separated into the blank control group, ER-L (25 μg/mL) group, ER-M (50 μg/mL) group, ER-H (75 μg/mL) group, and ER-H (75 μg/mL)+ PM (Hedgehog pathway activator, 1.5 μmol/L) group. MTT assay was applied to detect cell proliferative viability; the clonogenic ability of cells was detected by clonogenic assay; the abilities of cell migration and invasion were detected by scratch test and Transwell test; vascular mimicry test was applied to detect the ability of angiogenesis; WB assay was applied to detect the expressionof proteins related to EMT processes. Hedgehog signaling pathways, and mimic angiogenesis. Results: The proliferative viability of HT29 cells decreased gradually with the increase of ER concentration (P<0.05). Compared with the control group, cell clone formation rate, migration and invasion abilities,angiogenesis ability, the expressions of interstitial marker proteins (N-cadherin, vimentin), angiogenesis related proteins (VEGF, VE-cadherin) and hedgehog pathway related proteins (SHH, GLI1, SMO, c-Myc) in the various ER groups decreased, and the expressions of both epithelial marker protein (E-cadherin) and suppressor of fused protein (SUFU) in hedgehog pathway increased (all P<0.05). ER-H+PM group, to some extent, reversed the inhibition of ER on HT29 cell proliferation, EMT and angiogenesis(all P<0.05). Conclusion: ER can inhibit the proliferation, migration and invasion, EMT and angiogenesis of colorectal cancer HT29 cells, and its mechanism may be related to the inhibition of the activation of the Hedgehog signal pathway.