目的： 基于Hedgehog 信号通路探讨石斛提取物毛兰素（erianin，ER）抑制结直肠癌HT29 细胞上皮间质转化（EMT）和血管生成的作用机制。方法: 将HT29 细胞分为空白对照组、ER-L（25 μg/mL）组、ER-M（50 μg/mL）组、ER-H（75 μg/mL）组、 ER-H（75 μg/mL）+PM（Hedgehog 通路激活剂，1.5 μmol/L）组。MTT法检测细胞增殖活力，克隆形成实验检测细胞克隆形成能力，划痕实验和Transwell 实验检测细胞迁移与侵袭能力，血管拟态形成实验检测血管生成能力，WB法检测与EMT进程、Hedgehog信号通路和拟态血管生成相关蛋白质的表达。结果: HT29 细胞增殖活性随着ER质量浓度的升高而逐渐降低（P<0.05）；与空白对照组比较，ER各组细胞克隆形成率、迁移与侵袭能力、血管形成能力、间质标志蛋白（N-cadherin、vimentin）、血管生成相关蛋白（VEGF、VE-cadherin）及Hedgehog 通路相关蛋白（SHH、GLI1、SMO、c-Myc）表达均显著下降（均P<0.05），上皮标志蛋白（E-cadherin）、Hedgehog 通路中融合蛋白抑制剂（SUFU）蛋白表达均显著上升（均P<0.05）；PM 处理在一定程度上逆转了ER 对于HT29细胞增殖、EMT和血管生成的抑制作用（均P<0.05）。结论: ER可以抑制结直肠癌HT29细胞的增殖、迁移与侵袭、EMT和血管生成，其机制可能与抑制Hedgehog信号通路激活有关。

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.