RapamycinFungusV1, Main, Exploration, bibRecord, 000237

Short-Term Environmental Conditioning Enhances Tumorigenic Potential of Triple-Negative Breast Cancer Cells.

Identifieur interne : 000237 ( Main/Exploration ); précédent : 000236; suivant : 000238

Short-Term Environmental Conditioning Enhances Tumorigenic Potential of Triple-Negative Breast Cancer Cells.

Auteurs : Samantha S. Eckley [États-Unis] ; Johanna M. Buschhaus [États-Unis] ; Brock A. Humphries ; Tanner H. Robison [États-Unis] ; Kathryn E. Luker [États-Unis] ; Gary D. Luker [États-Unis]

Source :

Tomography (Ann Arbor, Mich.) [ 2379-139X ] ; 2019.

RBID : pubmed:31893233

Descripteurs français

English descriptors

KwdEn :
- Animals (MeSH), Carcinogenesis (MeSH), Cell Adhesion (MeSH), Cell Count (MeSH), Cell Line, Tumor (MeSH), Cell Proliferation (MeSH), Disease Models, Animal (MeSH), Disease Progression (MeSH), Epidermal Growth Factor (pharmacology), Extracellular Signal-Regulated MAP Kinases (pharmacology), Female (MeSH), Humans (MeSH), Luminescent Measurements (MeSH), Mechanistic Target of Rapamycin Complex 1 (antagonists & inhibitors), Neoplasm Metastasis (MeSH), Proto-Oncogene Proteins c-akt (pharmacology), Serum Albumin, Bovine (pharmacology), Sirolimus (analogs & derivatives), Sirolimus (pharmacology), Triple Negative Breast Neoplasms (pathology), Tumor Microenvironment (MeSH).
MESH :
- chemical , analogs & derivatives : Sirolimus.
- chemical , antagonists & inhibitors : Mechanistic Target of Rapamycin Complex 1.
- chemical , pharmacology : Epidermal Growth Factor, Extracellular Signal-Regulated MAP Kinases, Proto-Oncogene Proteins c-akt, Serum Albumin, Bovine, Sirolimus.
- pathology : Triple Negative Breast Neoplasms.
- Animals, Carcinogenesis, Cell Adhesion, Cell Count, Cell Line, Tumor, Cell Proliferation, Disease Models, Animal, Disease Progression, Female, Humans, Luminescent Measurements, Neoplasm Metastasis, Tumor Microenvironment.

Abstract

Tumor microenvironments expose cancer cells to heterogeneous, dynamic environments by shifting availability of nutrients, growth factors, and metabolites. Cells integrate various inputs to generate cellular memory that determines trajectories of subsequent phenotypes. Here we report that short-term exposure of triple-negative breast cancer cells to growth factors or targeted inhibitors regulates subsequent tumor initiation. Using breast cancer cells with different driver mutations, we conditioned cells lines with various stimuli for 4 hours before implanting these cells as tumor xenografts and quantifying tumor progression by means of bioluminescence imaging. In the orthotopic model, conditioning a low number of cancer cells with fetal bovine serum led to enhancement of tumor-initiating potential, tumor volume, and liver metastases. Epidermal growth factor and the mTORC1 inhibitor ridaforolimus produced similar but relatively reduced effects on tumorigenic potential. These data show that a short-term stimulus increases tumorigenic phenotypes based on cellular memory. Conditioning regimens failed to alter proliferation or adhesion of cancer cells in vitro or kinase signaling through Akt and ERK measured by multiphoton microscopy in vivo, suggesting that other mechanisms enhanced tumorigenesis. Given the dynamic nature of the tumor environment and time-varying concentrations of small-molecule drugs, this work highlights how variable conditions in tumor environments shape tumor formation, metastasis, and response to therapy.

DOI: 10.18383/j.tom.2019.00019
PubMed: 31893233
PubMed Central: PMC6935992

Affiliations:

Links toward previous steps (curation, corpus...)

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Le document en format XML

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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals (MeSH)</term>
<term>Carcinogenesis (MeSH)</term>
<term>Cell Adhesion (MeSH)</term>
<term>Cell Count (MeSH)</term>
<term>Cell Line, Tumor (MeSH)</term>
<term>Cell Proliferation (MeSH)</term>
<term>Disease Models, Animal (MeSH)</term>
<term>Disease Progression (MeSH)</term>
<term>Epidermal Growth Factor (pharmacology)</term>
<term>Extracellular Signal-Regulated MAP Kinases (pharmacology)</term>
<term>Female (MeSH)</term>
<term>Humans (MeSH)</term>
<term>Luminescent Measurements (MeSH)</term>
<term>Mechanistic Target of Rapamycin Complex 1 (antagonists & inhibitors)</term>
<term>Neoplasm Metastasis (MeSH)</term>
<term>Proto-Oncogene Proteins c-akt (pharmacology)</term>
<term>Serum Albumin, Bovine (pharmacology)</term>
<term>Sirolimus (analogs & derivatives)</term>
<term>Sirolimus (pharmacology)</term>
<term>Triple Negative Breast Neoplasms (pathology)</term>
<term>Tumor Microenvironment (MeSH)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Adhérence cellulaire (MeSH)</term>
<term>Animaux (MeSH)</term>
<term>Carcinogenèse (MeSH)</term>
<term>Complexe-1 cible mécanistique de la rapamycine (antagonistes et inhibiteurs)</term>
<term>Extracellular Signal-Regulated MAP Kinases (pharmacologie)</term>
<term>Facteur de croissance épidermique (pharmacologie)</term>
<term>Femelle (MeSH)</term>
<term>Humains (MeSH)</term>
<term>Lignée cellulaire tumorale (MeSH)</term>
<term>Mesures de luminescence (MeSH)</term>
<term>Microenvironnement tumoral (MeSH)</term>
<term>Modèles animaux de maladie humaine (MeSH)</term>
<term>Métastase tumorale (MeSH)</term>
<term>Numération cellulaire (MeSH)</term>
<term>Prolifération cellulaire (MeSH)</term>
<term>Protéines proto-oncogènes c-akt (pharmacologie)</term>
<term>Sirolimus (analogues et dérivés)</term>
<term>Sirolimus (pharmacologie)</term>
<term>Sérumalbumine bovine (pharmacologie)</term>
<term>Tumeurs du sein triple-négatives (anatomopathologie)</term>
<term>Évolution de la maladie (MeSH)</term>
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</keywords>
<keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>Mechanistic Target of Rapamycin Complex 1</term>
</keywords>
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<term>Extracellular Signal-Regulated MAP Kinases</term>
<term>Proto-Oncogene Proteins c-akt</term>
<term>Serum Albumin, Bovine</term>
<term>Sirolimus</term>
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<keywords scheme="MESH" qualifier="analogues et dérivés" xml:lang="fr"><term>Sirolimus</term>
</keywords>
<keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Tumeurs du sein triple-négatives</term>
</keywords>
<keywords scheme="MESH" qualifier="antagonistes et inhibiteurs" xml:lang="fr"><term>Complexe-1 cible mécanistique de la rapamycine</term>
</keywords>
<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Triple Negative Breast Neoplasms</term>
</keywords>
<keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Extracellular Signal-Regulated MAP Kinases</term>
<term>Facteur de croissance épidermique</term>
<term>Protéines proto-oncogènes c-akt</term>
<term>Sirolimus</term>
<term>Sérumalbumine bovine</term>
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<term>Carcinogenesis</term>
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<term>Cell Line, Tumor</term>
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<term>Disease Models, Animal</term>
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<term>Humans</term>
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<term>Carcinogenèse</term>
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<term>Humains</term>
<term>Lignée cellulaire tumorale</term>
<term>Mesures de luminescence</term>
<term>Microenvironnement tumoral</term>
<term>Modèles animaux de maladie humaine</term>
<term>Métastase tumorale</term>
<term>Numération cellulaire</term>
<term>Prolifération cellulaire</term>
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<front><div type="abstract" xml:lang="en">Tumor microenvironments expose cancer cells to heterogeneous, dynamic environments by shifting availability of nutrients, growth factors, and metabolites. Cells integrate various inputs to generate cellular memory that determines trajectories of subsequent phenotypes. Here we report that short-term exposure of triple-negative breast cancer cells to growth factors or targeted inhibitors regulates subsequent tumor initiation. Using breast cancer cells with different driver mutations, we conditioned cells lines with various stimuli for 4 hours before implanting these cells as tumor xenografts and quantifying tumor progression by means of bioluminescence imaging. In the orthotopic model, conditioning a low number of cancer cells with fetal bovine serum led to enhancement of tumor-initiating potential, tumor volume, and liver metastases. Epidermal growth factor and the mTORC1 inhibitor ridaforolimus produced similar but relatively reduced effects on tumorigenic potential. These data show that a short-term stimulus increases tumorigenic phenotypes based on cellular memory. Conditioning regimens failed to alter proliferation or adhesion of cancer cells in vitro or kinase signaling through Akt and ERK measured by multiphoton microscopy in vivo, suggesting that other mechanisms enhanced tumorigenesis. Given the dynamic nature of the tumor environment and time-varying concentrations of small-molecule drugs, this work highlights how variable conditions in tumor environments shape tumor formation, metastasis, and response to therapy.</div>
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<Abstract><AbstractText>Tumor microenvironments expose cancer cells to heterogeneous, dynamic environments by shifting availability of nutrients, growth factors, and metabolites. Cells integrate various inputs to generate cellular memory that determines trajectories of subsequent phenotypes. Here we report that short-term exposure of triple-negative breast cancer cells to growth factors or targeted inhibitors regulates subsequent tumor initiation. Using breast cancer cells with different driver mutations, we conditioned cells lines with various stimuli for 4 hours before implanting these cells as tumor xenografts and quantifying tumor progression by means of bioluminescence imaging. In the orthotopic model, conditioning a low number of cancer cells with fetal bovine serum led to enhancement of tumor-initiating potential, tumor volume, and liver metastases. Epidermal growth factor and the mTORC1 inhibitor ridaforolimus produced similar but relatively reduced effects on tumorigenic potential. These data show that a short-term stimulus increases tumorigenic phenotypes based on cellular memory. Conditioning regimens failed to alter proliferation or adhesion of cancer cells in vitro or kinase signaling through Akt and ERK measured by multiphoton microscopy in vivo, suggesting that other mechanisms enhanced tumorigenesis. Given the dynamic nature of the tumor environment and time-varying concentrations of small-molecule drugs, this work highlights how variable conditions in tumor environments shape tumor formation, metastasis, and response to therapy.</AbstractText>
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Short-Term Environmental Conditioning Enhances Tumorigenic Potential of Triple-Negative Breast Cancer Cells.

Short-Term Environmental Conditioning Enhances Tumorigenic Potential of Triple-Negative Breast Cancer Cells.

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