【摘要】 目的:研究CTNND1调控胰腺癌细胞增殖、迁移和侵袭的机制，为胰腺癌精准治疗提供新理论依据。方法:通过生信分析验证CTNND1在胰腺癌和正常组织中的表达，免疫组织化学(IHC)和qPCR进一步验证。Transwell、划痕实验和细胞增殖试验用于研究CTNND1对胰腺癌细胞增殖、迁移和侵袭的影响。裸鼠皮下成瘤实验检测CTNND1对人胰腺癌细胞成瘤能力的影响。结果:在胰腺癌细胞中敲低CTNND1可以抑制胰腺癌细胞的Wnt/β-catenin信号通路以及增殖、迁移和侵袭能力。加入LiCl(Wnt/β-catenin特异性激活剂)能部分恢复CTNND1敲低胰腺癌细胞的增殖、迁移和侵袭能力。裸鼠皮下成瘤显示，敲低CTNND1抑制了肿瘤裸鼠皮下成瘤。结论:敲低CTNND1能从体内外通过Wnt/β-catenin信号通路调控胰腺癌的增殖、迁移和侵袭及皮下成瘤能力。更多还原

【Abstract】 Objective:To study the knockdown of CTNND1 through Wnt/β-catenin signaling pathway regulates the proliferation, migration and invasion of pancreatic cancer cells, and further provides theoretical basis for molecular targeted therapy in pancreatic cancer.Methods:The expression of CTNND1 in pancreatic cancer and normal tissues was validated through bioinformatics analysis, and further confirmed by immunohistochemistry(IHC) and qPCR.Transwell, wound healing, and cell proliferation assays were conducted to investigate the impact of CTNND1 on the proliferation, migration, and invasion of pancreatic cancer cells.Subcutaneous tumor formation experiments in nude mice were performed to assess the tumorigenic ability of human pancreatic cancer cells with altered CTNND1 expression.Results:Knockdown of CTNND1 in pancreatic cancer cells inhibited the Wnt/β-catenin signaling pathway as well as the proliferation, migration, and invasion capabilities of these cells.Adding of LiCl(a specific activator of Wnt/β-catenin) partially restored the proliferation, migration, and invasion capabilities of CTNND1-knockdown pancreatic cancer cells.Subcutaneous tumor formation in nude mice demonstrated that CTNND1 knockdown suppressed tumor growth.Conclusion:Knockdown of CTNND1 can regulate the proliferation, migration, invasion, and subcutaneous tumor formation ability of pancreatic cancer through the Wnt/β-catenin signaling pathway, both in vitro and in vivo.更多还原