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用于研究肿瘤微环境中癌细胞细胞串扰的气液器官型测定法。

Air-liquid organotypic assays to investigate cellular crosstalk in the tumor microenvironment of cancer cells.

机构信息

Department of Pathology and Laboratory Medicine, Weill Cornell Medicine, New York, NY 10065, USA.

Department of Pathology and Laboratory Medicine, Weill Cornell Medicine, New York, NY 10065, USA.

出版信息

STAR Protoc. 2022 Aug 18;3(3):101635. doi: 10.1016/j.xpro.2022.101635. eCollection 2022 Sep 16.

DOI:10.1016/j.xpro.2022.101635
PMID:36035805
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9405995/
Abstract

Air-liquid organotypic culture models enable the study of the cellular crosstalk in the tumor microenvironment. This 3D assay recapitulates the tumor niche more faithfully than 2D culture systems and represents a versatile platform that can be easily adapted to different types of cancer cells, stromal components, or ECM composition. Here, we detail the steps to build an organotypic culture including the preparation of the organotypic structure, organotypic gels, cell seeding, gel casting, membrane processing, and image and data analysis. For complete details on the use and execution of this protocol, please refer to Linares et al. (2022).

摘要

气液型器官培养模型可用于研究肿瘤微环境中的细胞串扰。与 2D 培养系统相比,这种 3D 检测更能真实地再现肿瘤微环境,是一种灵活的平台,可以很容易地适应不同类型的癌细胞、基质成分或细胞外基质组成。在这里,我们详细介绍了构建器官培养模型的步骤,包括器官样结构的准备、器官样凝胶、细胞接种、凝胶铸造、膜处理以及图像和数据分析。有关该方案使用和执行的完整详细信息,请参考 Linares 等人(2022 年)的文献。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/70e9/9405995/6249b501a665/gr8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/70e9/9405995/6c43de454b46/fx1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/70e9/9405995/6071fb180cfd/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/70e9/9405995/5331a5e08812/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/70e9/9405995/4106a8ae010e/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/70e9/9405995/0ab0bee222f5/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/70e9/9405995/81974cdbf8a5/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/70e9/9405995/2422653e9e3b/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/70e9/9405995/8f21dac9d004/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/70e9/9405995/6249b501a665/gr8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/70e9/9405995/6c43de454b46/fx1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/70e9/9405995/6071fb180cfd/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/70e9/9405995/5331a5e08812/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/70e9/9405995/4106a8ae010e/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/70e9/9405995/0ab0bee222f5/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/70e9/9405995/81974cdbf8a5/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/70e9/9405995/2422653e9e3b/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/70e9/9405995/8f21dac9d004/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/70e9/9405995/6249b501a665/gr8.jpg

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本文引用的文献

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Metabolic reprogramming of stromal fibroblasts through p62-mTORC1 signaling promotes inflammation and tumorigenesis.
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