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技术文章
CDCA8/SNAI2复合物激活CD44促进胰腺导管腺癌的增殖和侵袭
点击次数：2714 发布时间：2024/12/26 16:57:47
2022年9月，复旦大学华山医院胰腺外科；复旦大学胰腺疾病研究所(Department of Pancreatic Surgery, Huashan Hospital, Fudan University, Shanghai 200040, China；Pancreatic Disease Institute, Fudan University, Shanghai 200040, China)Ji Li老师研究团队在《Cancers》上发表论文：
“CDCA8/SNAI2 Complex Activates CD44 to Promote Proliferation and Invasion of Pancreatic Ductal Adenocarcinoma”
“CDCA8/SNAI2复合物激活CD44促进胰腺导管腺癌的增殖和侵袭”
Abstract：
Background: Recently, cell division cycle associated 8 (CDCA8) was found to be overexpressed in pancreatic ductal adenocarcinoma (PDAC). Here, we aimed to explore the specific mechanism of action of CDCA8 in PDAC progression. (2) Methods: All human PDAC samples and clinical data were collected from Huashan Hospital, Fudan University. All experimental studies were carried out using many in vitro and in vivo assays, including lentiviral transfection, real-time quantitative polymerase chain reaction (qPCR), western blotting, co-immunoprecipitation (Co-IP), chromatin IP (ChIP)-qPCR, dual-luciferase reporter, and in vivo imaging assays. (3) Results: Clinical data analysis of human PDAC samples revealed that CDCA8 overexpression were positively and negatively associated with tumor grade (p = 0.007) and overall survival (p = 0.045), respectively. CDCA8 knockdown inhibited PDAC proliferation and invasion in in vitro and in vivo assays. CD44 was also up-regulated by CDCA8 during PDAC progression. CDCA8 could be combined with SNAI2 to form a CDCA8/SNAI2 complex to integrate with the CD44 promoter as indicated through ChIP-qPCR and dual-luciferase reporter assays. (4) Conclusion: We showed that CDCA8-CD44 axis plays a key role in the proliferation and invasion of PDAC, which provides a potential target for treatment.
摘要：
背景:近年来，细胞分裂周期相关蛋白8 (CDCA8)在胰腺导管腺癌(PDAC)中被发现过表达。在这里，我们旨在探讨CDCA8在PDAC进展中的具体作用机制。(2)方法:所有人类PDAC样本及临床资料均来自复旦大学华山医院。所有实验研究均采用多种体外和体内检测方法进行，包括慢病毒转染、实时定量聚合酶链反应(qPCR)、western blotting、共免疫沉淀(Co-IP)、染色质IP (ChIP)-qPCR、双荧光素酶报告基因和体内成像检测。(3)结果:人类PDAC样本的临床数据分析显示，CDCA8过表达与肿瘤分级(p = 0.007)和总生存率(p = 0.045)分别呈正相关和负相关。在体外和体内实验中，敲低CDCA8抑制PDAC的增殖和侵袭。在PDAC进展过程中，CD44也被CDCA8上调。通过ChIP-qPCR和双荧光素酶报告基因检测表明，CDCA8可以与SNAI2结合形成CDCA8/SNAI2复合物，并与CD44启动子整合。(4)结论:我们发现CDCA8-CD44轴在PDAC的增殖和侵袭中起关键作用，为PDAC的治疗提供了潜在的靶点。
该论文中，人PDAC细胞系PANC-1、ws -1990、AsPC-1和BxPC-3以及人胰腺导管上皮细胞系HPDE6-C7细胞是使用Ausbian进口特级胎牛血清完成的。欲了解或购买Ausbian系列血清可以联系北京缔一生物400-166-8600.
原创作者：北京缔一生物科技有限公司
