Receptor Interactive Protein Kinase 3 Promotes Cisplatin-Triggered Necrosis in Apoptosis-Resistant Esophageal Squamous Cell Carcinoma Cells
Identifieur interne : 001745 ( Main/Exploration ); précédent : 001744; suivant : 001746Receptor Interactive Protein Kinase 3 Promotes Cisplatin-Triggered Necrosis in Apoptosis-Resistant Esophageal Squamous Cell Carcinoma Cells
Auteurs : Yang Xu [République populaire de Chine] ; Zhengwei Lin [République populaire de Chine] ; Nan Zhao [République populaire de Chine] ; Lanping Zhou [République populaire de Chine] ; Fang Liu [République populaire de Chine] ; Zbigniew Cichacz [États-Unis] ; Lin Zhang [États-Unis] ; Qimin Zhan [République populaire de Chine] ; Xiaohang Zhao [République populaire de Chine]Source :
- PLoS ONE [ 1932-6203 ] ; 2014.
Descripteurs français
- KwdFr :
- Animaux, Antinéoplasiques (pharmacologie), Apoptose (), Apoptose (génétique), Carcinome épidermoïde (anatomopathologie), Carcinome épidermoïde (génétique), Carcinome épidermoïde (métabolisme), Charge tumorale (), Charge tumorale (génétique), Cisplatine (pharmacologie), Facteur de nécrose tumorale alpha (biosynthèse), Humains, Interférence par ARN, Lignée cellulaire tumorale, Modèles animaux de maladie humaine, Nécrose (), Nécrose (génétique), Protéines et peptides de signalisation intracellulaire (déficit), Protéines mitochondriales (déficit), Receptor-Interacting Protein Serine-Threonine Kinases (génétique), Receptor-Interacting Protein Serine-Threonine Kinases (métabolisme), Régulation de l'expression des gènes tumoraux (), Souris, Techniques de knock-out de gènes, Tests d'activité antitumorale sur modèle de xénogreffe, Transduction du signal, Tumeurs de l'oesophage (anatomopathologie), Tumeurs de l'oesophage (génétique), Tumeurs de l'oesophage (métabolisme).
- MESH :
- anatomopathologie : Carcinome épidermoïde, Tumeurs de l'oesophage.
- biosynthèse : Facteur de nécrose tumorale alpha.
- déficit : Protéines et peptides de signalisation intracellulaire, Protéines mitochondriales.
- génétique : Apoptose, Carcinome épidermoïde, Charge tumorale, Nécrose, Receptor-Interacting Protein Serine-Threonine Kinases, Tumeurs de l'oesophage.
- métabolisme : Carcinome épidermoïde, Receptor-Interacting Protein Serine-Threonine Kinases, Tumeurs de l'oesophage.
- pharmacologie : Antinéoplasiques, Cisplatine.
- Animaux, Apoptose, Charge tumorale, Humains, Interférence par ARN, Lignée cellulaire tumorale, Modèles animaux de maladie humaine, Nécrose, Régulation de l'expression des gènes tumoraux, Souris, Techniques de knock-out de gènes, Tests d'activité antitumorale sur modèle de xénogreffe, Transduction du signal.
English descriptors
- KwdEn :
- Animals, Antineoplastic Agents (pharmacology), Apoptosis (drug effects), Apoptosis (genetics), Carcinoma, Squamous Cell (genetics), Carcinoma, Squamous Cell (metabolism), Carcinoma, Squamous Cell (pathology), Cell Line, Tumor, Cisplatin (pharmacology), Disease Models, Animal, Esophageal Neoplasms (genetics), Esophageal Neoplasms (metabolism), Esophageal Neoplasms (pathology), Gene Expression Regulation, Neoplastic (drug effects), Gene Knockout Techniques, Humans, Intracellular Signaling Peptides and Proteins (deficiency), Mice, Mitochondrial Proteins (deficiency), Necrosis (chemically induced), Necrosis (genetics), RNA Interference, Receptor-Interacting Protein Serine-Threonine Kinases (genetics), Receptor-Interacting Protein Serine-Threonine Kinases (metabolism), Signal Transduction, Tumor Burden (drug effects), Tumor Burden (genetics), Tumor Necrosis Factor-alpha (biosynthesis), Xenograft Model Antitumor Assays.
- MESH :
- chemical , biosynthesis : Tumor Necrosis Factor-alpha.
- chemical , deficiency : Intracellular Signaling Peptides and Proteins, Mitochondrial Proteins.
- chemical , genetics : Receptor-Interacting Protein Serine-Threonine Kinases.
- chemical , metabolism : Receptor-Interacting Protein Serine-Threonine Kinases.
- chemical , pharmacology : Antineoplastic Agents, Cisplatin.
- chemically induced : Necrosis.
- drug effects : Apoptosis, Gene Expression Regulation, Neoplastic, Tumor Burden.
- genetics : Apoptosis, Carcinoma, Squamous Cell, Esophageal Neoplasms, Necrosis, Tumor Burden.
- metabolism : Carcinoma, Squamous Cell, Esophageal Neoplasms.
- pathology : Carcinoma, Squamous Cell, Esophageal Neoplasms.
- Animals, Cell Line, Tumor, Disease Models, Animal, Gene Knockout Techniques, Humans, Mice, RNA Interference, Signal Transduction, Xenograft Model Antitumor Assays.
Abstract
Cisplatin-based chemotherapy is currently the standard treatment for locally advanced esophageal cancer. Cisplatin has been shown to induce both apoptosis and necrosis in cancer cells, but the mechanism by which programmed necrosis is induced remains unknown. In this study, we provide evidence that cisplatin induces necrotic cell death in apoptosis-resistant esophageal cancer cells. This cell death is dependent on RIPK3 and on necrosome formation via autocrine production of TNFα. More importantly, we demonstrate that RIPK3 is necessary for cisplatin-induced killing of esophageal cancer cells because inhibition of RIPK1 activity by necrostatin or knockdown of RIPK3 significantly attenuates necrosis and leads to cisplatin resistance. Moreover, microarray analysis confirmed an anti-apoptotic molecular expression pattern in esophageal cancer cells in response to cisplatin. Taken together, our data indicate that RIPK3 and autocrine production of TNFα contribute to cisplatin sensitivity by initiating necrosis when the apoptotic pathway is suppressed or absent in esophageal cancer cells. These data provide new insight into the molecular mechanisms underlying cisplatin-induced necrosis and suggest that RIPK3 is a potential marker for predicting cisplatin sensitivity in apoptosis-resistant and advanced esophageal cancer.
Url:
DOI: 10.1371/journal.pone.0100127
PubMed: 24959694
PubMed Central: 4069059
Affiliations:
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Le document en format XML
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<term>Antineoplastic Agents (pharmacology)</term>
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<term>Apoptosis (genetics)</term>
<term>Carcinoma, Squamous Cell (genetics)</term>
<term>Carcinoma, Squamous Cell (metabolism)</term>
<term>Carcinoma, Squamous Cell (pathology)</term>
<term>Cell Line, Tumor</term>
<term>Cisplatin (pharmacology)</term>
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<term>RNA Interference</term>
<term>Receptor-Interacting Protein Serine-Threonine Kinases (genetics)</term>
<term>Receptor-Interacting Protein Serine-Threonine Kinases (metabolism)</term>
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<term>Tumor Burden (drug effects)</term>
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<term>Xenograft Model Antitumor Assays</term>
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<keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term>
<term>Antinéoplasiques (pharmacologie)</term>
<term>Apoptose ()</term>
<term>Apoptose (génétique)</term>
<term>Carcinome épidermoïde (anatomopathologie)</term>
<term>Carcinome épidermoïde (génétique)</term>
<term>Carcinome épidermoïde (métabolisme)</term>
<term>Charge tumorale ()</term>
<term>Charge tumorale (génétique)</term>
<term>Cisplatine (pharmacologie)</term>
<term>Facteur de nécrose tumorale alpha (biosynthèse)</term>
<term>Humains</term>
<term>Interférence par ARN</term>
<term>Lignée cellulaire tumorale</term>
<term>Modèles animaux de maladie humaine</term>
<term>Nécrose ()</term>
<term>Nécrose (génétique)</term>
<term>Protéines et peptides de signalisation intracellulaire (déficit)</term>
<term>Protéines mitochondriales (déficit)</term>
<term>Receptor-Interacting Protein Serine-Threonine Kinases (génétique)</term>
<term>Receptor-Interacting Protein Serine-Threonine Kinases (métabolisme)</term>
<term>Régulation de l'expression des gènes tumoraux ()</term>
<term>Souris</term>
<term>Techniques de knock-out de gènes</term>
<term>Tests d'activité antitumorale sur modèle de xénogreffe</term>
<term>Transduction du signal</term>
<term>Tumeurs de l'oesophage (anatomopathologie)</term>
<term>Tumeurs de l'oesophage (génétique)</term>
<term>Tumeurs de l'oesophage (métabolisme)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="biosynthesis" xml:lang="en"><term>Tumor Necrosis Factor-alpha</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="deficiency" xml:lang="en"><term>Intracellular Signaling Peptides and Proteins</term>
<term>Mitochondrial Proteins</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Receptor-Interacting Protein Serine-Threonine Kinases</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Receptor-Interacting Protein Serine-Threonine Kinases</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Antineoplastic Agents</term>
<term>Cisplatin</term>
</keywords>
<keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Carcinome épidermoïde</term>
<term>Tumeurs de l'oesophage</term>
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<keywords scheme="MESH" qualifier="biosynthèse" xml:lang="fr"><term>Facteur de nécrose tumorale alpha</term>
</keywords>
<keywords scheme="MESH" qualifier="chemically induced" xml:lang="en"><term>Necrosis</term>
</keywords>
<keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Apoptosis</term>
<term>Gene Expression Regulation, Neoplastic</term>
<term>Tumor Burden</term>
</keywords>
<keywords scheme="MESH" qualifier="déficit" xml:lang="fr"><term>Protéines et peptides de signalisation intracellulaire</term>
<term>Protéines mitochondriales</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Apoptosis</term>
<term>Carcinoma, Squamous Cell</term>
<term>Esophageal Neoplasms</term>
<term>Necrosis</term>
<term>Tumor Burden</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Apoptose</term>
<term>Carcinome épidermoïde</term>
<term>Charge tumorale</term>
<term>Nécrose</term>
<term>Receptor-Interacting Protein Serine-Threonine Kinases</term>
<term>Tumeurs de l'oesophage</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Carcinoma, Squamous Cell</term>
<term>Esophageal Neoplasms</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Carcinome épidermoïde</term>
<term>Receptor-Interacting Protein Serine-Threonine Kinases</term>
<term>Tumeurs de l'oesophage</term>
</keywords>
<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Carcinoma, Squamous Cell</term>
<term>Esophageal Neoplasms</term>
</keywords>
<keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Antinéoplasiques</term>
<term>Cisplatine</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Cell Line, Tumor</term>
<term>Disease Models, Animal</term>
<term>Gene Knockout Techniques</term>
<term>Humans</term>
<term>Mice</term>
<term>RNA Interference</term>
<term>Signal Transduction</term>
<term>Xenograft Model Antitumor Assays</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Animaux</term>
<term>Apoptose</term>
<term>Charge tumorale</term>
<term>Humains</term>
<term>Interférence par ARN</term>
<term>Lignée cellulaire tumorale</term>
<term>Modèles animaux de maladie humaine</term>
<term>Nécrose</term>
<term>Régulation de l'expression des gènes tumoraux</term>
<term>Souris</term>
<term>Techniques de knock-out de gènes</term>
<term>Tests d'activité antitumorale sur modèle de xénogreffe</term>
<term>Transduction du signal</term>
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<front><div type="abstract" xml:lang="en"><p>Cisplatin-based chemotherapy is currently the standard treatment for locally advanced esophageal cancer. Cisplatin has been shown to induce both apoptosis and necrosis in cancer cells, but the mechanism by which programmed necrosis is induced remains unknown. In this study, we provide evidence that cisplatin induces necrotic cell death in apoptosis-resistant esophageal cancer cells. This cell death is dependent on RIPK3 and on necrosome formation via autocrine production of TNFα. More importantly, we demonstrate that RIPK3 is necessary for cisplatin-induced killing of esophageal cancer cells because inhibition of RIPK1 activity by necrostatin or knockdown of RIPK3 significantly attenuates necrosis and leads to cisplatin resistance. Moreover, microarray analysis confirmed an anti-apoptotic molecular expression pattern in esophageal cancer cells in response to cisplatin. Taken together, our data indicate that RIPK3 and autocrine production of TNFα contribute to cisplatin sensitivity by initiating necrosis when the apoptotic pathway is suppressed or absent in esophageal cancer cells. These data provide new insight into the molecular mechanisms underlying cisplatin-induced necrosis and suggest that RIPK3 is a potential marker for predicting cisplatin sensitivity in apoptosis-resistant and advanced esophageal cancer.</p>
</div>
</front>
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</TEI>
<affiliations><list><country><li>République populaire de Chine</li>
<li>États-Unis</li>
</country>
<region><li>Arizona</li>
<li>Pennsylvanie</li>
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<settlement><li>Pékin</li>
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<name sortKey="Liu, Fang" sort="Liu, Fang" uniqKey="Liu F" first="Fang" last="Liu">Fang Liu</name>
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</tree>
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