检索结果-南通市图书馆

Uncoupling protein 2 deficiency of non-cancerous tissues inhibits the progression of pancreatic cancer in mice

Hepatobiliary & Pancreatic Diseases International 2023年第2期22卷 190-199页

作者： Denis Revskij Jakob Runst Camilla Umstätter Luise Ehlers Sarah Rohde Dietmar Zechner Manuela Bastian Brigitte Müller-Hilke georg fuellen Larissa Henze Hugo Murua Escobar Christian Junghanss Axel Kowald Uwe Walter Rüdiger Köhling Olaf Wolkenhauer Robert Jaster Department of Medicine Ⅱ Division of GastroenterologyRostock University Medical CenterRostockGermany Rudolf-Zenker-Institute of Experimental Surgery Rostock University Medical CenterRostockGermany Institute of Clinical Chemistry and Laboratory Medicine Rostock University Medical CenterRostockGermany Facility for Cell Sorting and Cell Analysis and Institute of Immunology Rostock University Medical CenterRostockGermany Institute for Biostatistics and Informatics in Medicine and Ageing Research Rostock University Medical CenterRostockGermany Department of Medicine Clinic ⅢHematologyOncologyPalliative MedicineRostock University Medical CenterRostockGermany Department of Neurology Rostock University Medical CenterRostockGermany Oscar LangendorffInstitute of Physiology Rostock University Medical CenterRostockGermany Department of Systems Biology and Bioinformatics University of RostockRostockGermany

Background: Pancreatic ductal adenocarcinoma(PDAC) is a disease of the elderly mostly because its development from preneoplastic lesions depends on the accumulation of gene mutations and epigenetic alterations over time. How aging of non-cancerous tissues of the host affects tumor progression, however, remains largely unknown. Methods: We took advantage of a model of accelerated aging, uncoupling protein 2-deficient( Ucp2 knockout, Ucp2 KO) mice, to investigate the growth of orthotopically transplanted Ucp2 wild-type(WT) PDAC cells(cell lines Panc02 and 6606PDA) in vivo and to study strain-dependent differences of the PDAC microenvironment. Results: Measurements of tumor weights and quantification of proliferating cells indicated a significant growth advantage of Panc02 and 6606PDA cells in WT mice compared to Ucp2 KO mice. In tumors in the knockout strain, higher levels of interferon-γ m RNA despite similar numbers of tumor-infiltrating T cells were observed. 6606PDA cells triggered a stronger stromal reaction in Ucp2 KO mice than in WT animals. Accordingly, pancreatic stellate cells from Ucp2 KO mice proliferated at a higher rate than cells of the WT strain when they were incubated with conditioned media from PDAC cells. Conclusions: Ucp2 modulates PDAC microenvironment in a way that favors tumor progression and implicates an altered stromal response as one of the underlying mechanisms.

关键词： Pancreatic cancer Orthotopic model Uncoupling protein 2 Fibrosis

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

欢迎您,

建议与咨询留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

时间限定

文献类型

馆藏选择

核心期刊

语言

文献类型

帮助

文字说明：

检索规则说明：

检索范例：

分类表

所选分类

限定检索结果

文献类型

馆藏范围

日期分布

学科分类号

主题

机构

作者

语言

在线全文

请选择保存的检索档案：

请选择收藏分类：

通借通还

欢迎您,

建议与咨询 留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

时间限定

文献类型

馆藏选择

核心期刊

语言

文献类型

帮助

文字说明：

检索规则说明：

检索范例：

分类表

所选分类

限定检索结果

文献类型

馆藏范围

日期分布

学科分类号

主题

机构

作者

语言

在线全文

请选择保存的检索档案： 新增检索档案 确定 取消

请选择收藏分类： 新增自定义分类 确定 取消

通借通还

建议与咨询留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

请选择保存的检索档案：

请选择收藏分类：