目的：探究C-藻蓝蛋白（C-phycocyanin，C-PC）对转化生长因子β1（transforming growth factor beta 1，TGF-β1）诱导的 宫颈癌Caski细胞上皮-间充质转化（epithelial-mesenchymal transition, EMT）的影响。方法：根据处理方法不同将Caski细胞分为 3组即10 ng/ml TGF-β1处理组、 10 ng/ml TGF-β1+300 μg/ml C-PC共处理组和对照组（未加药处理），处理24 h后观察细胞的形态 变化；采用划痕实验及Transwell实验分别检测TGF-β1和C-PC对Caski细胞迁移和侵袭的影响；Western blotting方法检测C-PC 对TGF-β1诱导的Caski细胞上皮表型标志蛋白E-cadherin、间质表型标志蛋白N-cadherin表达水平的影响；qPCR 法检测间质表 型相关锌指转录因子Snail、Zeb1、Twist mRNA的表达。结果：TGF-β1处理组Caski细胞失去原有的上皮表型的特征， 而TGF-β 1+C-PC共处理组细胞保持正常的上皮表型的特征；TGF-β1处理组Caski细胞的迁移率[（60.0±1.4） % vs（33.5±2.2） %、（40.0± 2.8） %， 均P<0.05]和侵袭穿膜细胞数[（108.2±6.2）vs（25.2±3.1）、（39.8±5.4）个， 均P<0.01]较共处理组和对照组显著升高；与对照 组相比，TGF-β1处理组Caski细胞中E-cadherin表达显著降低（P<0.05），Twist、Snail、Zeb1的mRNA表达水平显著升高（P<0.01）， 而加入C-PC共处理可逆转上述改变（P<0.05或P<0.01），同时显著降低N-cadherin的蛋白表达水平（均P<0.05）。结论：C-PC处 理能够抑制TGF-β1诱导的Caski细胞侵袭转移能力进而影响EMT过程，其机制可能与C-PC处理降低Twist、Snail、Zeb1的 mRNA表达有关。

Objective: To investigate the effect of C-phycocyanin (C-PC) on the epithelial-mesenchymal transition (EMT) of cervical cancer Caski cells induced by transforming growth factor beta1 (TGF-β1). Methods: According to different treatment methods, Caski cells were divided into three groups: 10 ng/ml TGF-β1 treatment group, 10 ng/ml TGF-β1+300 μg/ml C-PC co-treatment group and control group (untreated). After 24 h of treatment, the morphological changes of Caski cells were observed, and the effects of TGF-β1 and C-PC on the migration and invasion of Caski cells were detected by Scratch test and Transwell test, respectively. Western blotting was used to detect the effect of C-PC on the expression of epithelial phenotypic marker protein E-cadherin and stromal phenotypic marker protein N-cadherin in TGF-β1-induced Caski cells, and qPCR was used to detect the mRNA expressions of EMT related factors Snail, Zeb1 and Twist. Results: Caski cells in the TGF-β1 treatment group lost the characteristics of the original epithelial phenotype, while the cells in the TGF-β1+C-PC co-treatment group maintained the characteristics of normal epithelial phenotype; the migration rate ([60.0±1.4]% vs [33.5±2.2]%, [40.0±2.8]%, both P<0.05) and the number of invasive transmembrane cells ([108.2±6.2] vs [25.2±3.1], [39.8±5.4], both P<0.01]) of Caski cells in the TGF- β1 treatment group were significantly higher than those in the co-treatment group and the control group. Compared with the control group, the expression of E-cadherin in Caski cells treated with TGF-β1 decreased sig ·· nificantly (P<0.05), while the mRNA expressions of Twist, Snail and Zeb1 increased significantly (all P<0.05); However, co-treatment with C-PC reversed above changes (P<0.05 or P<0.01), and significantly decreased the protein expression level of N-cadherin (P< 0.05). Conclusion: C-PC treatment can inhibit the invasion and metastasis ability of Caski cells induced by TGF-β1 and further affects the EMT process. The mechanism may be related to the decrease of mRNAexpressions of Twist, Snail and Zeb1 by C-PC treatment.

国家自然科学基金资助项目（No.81871231，81471546，81001346）；山东省高等学校青年创新科技计划资助（No.2019KJK016) ；青岛 市民生科技计划项目资助（No.18-6-1-91-nsh）