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Your search keyword '"Krotenberg Garcia A."' showing total 4 results
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4 results on '"Krotenberg Garcia A."'

1. Generation of mixed murine organoids to model cellular interactions.

Author

Krotenberg Garcia A, van Rheenen J, and Suijkerbuijk SJE

Subjects
Animals, Cell Culture Techniques, Cells, Cultured, Mice, Cell Communication physiology, Organoids cytology, Tissue Culture Techniques methods
Abstract

Cell competition is a mechanism of interaction that dictates cell selection based on differences in cellular fitness. We designed a protocol to generate mixed murine organoids and enteroid monolayers used to study such complex cellular interactions in a mammalian system. This protocol is dedicated to follow the behavior of different cell populations over time, using (time-lapse) microscopy or transcriptome/proteome analysis. For complete details on the use and execution of this protocol, please refer to Krotenberg Garcia et al. (2021)., Competing Interests: The authors declare no competing interests., (© 2021 The Author(s).)

Published
2021
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2. Active elimination of intestinal cells drives oncogenic growth in organoids.

Author

Krotenberg Garcia A, Fumagalli A, Le HQ, Jackstadt R, Lannagan TRM, Sansom OJ, van Rheenen J, and Suijkerbuijk SJE

Subjects
Animals, Apoptosis, Carcinogenesis metabolism, Cell Competition, Cell Line, Tumor, Fetus pathology, MAP Kinase Signaling System, Male, Mice, Inbred C57BL, Mice, Transgenic, Organoids metabolism, Receptors, G-Protein-Coupled metabolism, Stem Cells metabolism, Mice, Carcinogenesis pathology, Intestines pathology, Organoids pathology
Abstract

Competitive cell interactions play a crucial role in quality control during development and homeostasis. Here, we show that cancer cells use such interactions to actively eliminate wild-type intestine cells in enteroid monolayers and organoids. This apoptosis-dependent process boosts proliferation of intestinal cancer cells. The remaining wild-type population activates markers of primitive epithelia and transits to a fetal-like state. Prevention of this cell-state transition avoids elimination of wild-type cells and, importantly, limits the proliferation of cancer cells. Jun N-terminal kinase (JNK) signaling is activated in competing cells and is required for cell-state change and elimination of wild-type cells. Thus, cell competition drives growth of cancer cells by active out-competition of wild-type cells through forced cell death and cell-state change in a JNK-dependent manner., Competing Interests: Declaration of interests H.Q.L. is employed by Boehringer Ingelheim Pharma GmbH & Co. KG., (Copyright © 2021 The Authors. Published by Elsevier Inc. All rights reserved.)

Published
2021
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3. Generation of mixed murine organoids to model cellular interactions

Author

Ana Krotenberg Garcia, Jacco van Rheenen, and Saskia Jacoba Elisabeth Suijkerbuijk

Subjects
Cancer, Cell Biology, Cell culture, Microscopy, Organoids, Science (General), Q1-390
Abstract

Summary: Cell competition is a mechanism of interaction that dictates cell selection based on differences in cellular fitness. We designed a protocol to generate mixed murine organoids and enteroid monolayers used to study such complex cellular interactions in a mammalian system. This protocol is dedicated to follow the behavior of different cell populations over time, using (time-lapse) microscopy or transcriptome/proteome analysis.For complete details on the use and execution of this protocol, please refer to Krotenberg Garcia et al. (2021).

Published
2021
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4. Active elimination of intestinal cells drives oncogenic growth in organoids

Author

Owen J. Sansom, Huy Quang Le, Jacco van Rheenen, Arianna Fumagalli, Rene Jackstadt, Tamsin Rosemary Margaret Lannagan, Saskia J.E. Suijkerbuijk, and Ana Krotenberg Garcia

Subjects
Male, Programmed cell death, Carcinogenesis, MAP Kinase Signaling System, Population, Cell, Apoptosis, Mice, Transgenic, General Biochemistry, Genetics and Molecular Biology, Article, Receptors, G-Protein-Coupled, Fetus, Cell Line, Tumor, Organoid, medicine, Animals, cancer, education, education.field_of_study, Kinase, Chemistry, Stem Cells, Cancer, medicine.disease, Cell biology, Intestines, Mice, Inbred C57BL, Organoids, medicine.anatomical_structure, Cell Competition, Cancer cell, fetal-like, JNK, small intestine, Homeostasis
Abstract

Summary Competitive cell interactions play a crucial role in quality control during development and homeostasis. Here, we show that cancer cells use such interactions to actively eliminate wild-type intestine cells in enteroid monolayers and organoids. This apoptosis-dependent process boosts proliferation of intestinal cancer cells. The remaining wild-type population activates markers of primitive epithelia and transits to a fetal-like state. Prevention of this cell-state transition avoids elimination of wild-type cells and, importantly, limits the proliferation of cancer cells. Jun N-terminal kinase (JNK) signaling is activated in competing cells and is required for cell-state change and elimination of wild-type cells. Thus, cell competition drives growth of cancer cells by active out-competition of wild-type cells through forced cell death and cell-state change in a JNK-dependent manner., Graphical abstract, Highlights • In organoids, wild-type intestine cells are actively eliminated by cancer cells • Cell competition boosts proliferation of intestinal cancer cells • Remaining wild-type cells adopt a fetal-like state • JNK signaling in wild-type cells drives cell competition, Interactions between cells helps coordinated decision making in tissues. Krotenberg Garcia et al. show that intestinal cancer cells use competitive cell interactions to actively eliminate surrounding wild-type cells. These interactions drive oncogenic growth in organoids.

Published
2020

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