Regulation of autophagy and chloroquine sensitivity by oncogenic RAS in vitro is context-dependent.
Identifieur interne : 000258 ( Ncbi/Checkpoint ); précédent : 000257; suivant : 000259Regulation of autophagy and chloroquine sensitivity by oncogenic RAS in vitro is context-dependent.
Auteurs : Michael J. Morgan [États-Unis] ; Graciela Gamez [États-Unis] ; Christina Menke [États-Unis] ; Ariel Hernandez [États-Unis] ; Jacqueline Thorburn [États-Unis] ; Freddi Gidan [États-Unis] ; Leah Staskiewicz [États-Unis] ; Shellie Morgan [États-Unis] ; Christopher Cummings [États-Unis] ; Paola Maycotte [États-Unis] ; Andrew Thorburn [États-Unis]Source :
- Autophagy [ 1554-8635 ] ; 2014.
Descripteurs français
- KwdFr :
- MESH :
- anatomopathologie : Tumeurs du poumon.
- métabolisme : Phagosomes, Protéine p53 suppresseur de tumeur, Protéines G ras.
- pharmacologie : Chloroquine.
- Autophagie, Cellules HEK293, Humains, Lignée cellulaire tumorale, Oncogènes, Phagosomes, Prolifération cellulaire.
English descriptors
- KwdEn :
- MESH :
- chemical , metabolism : Tumor Suppressor Protein p53, ras Proteins.
- chemical , pharmacology : Chloroquine.
- drug effects : Autophagy, Cell Proliferation, Phagosomes.
- metabolism : Phagosomes.
- pathology : Lung Neoplasms.
- Cell Line, Tumor, HEK293 Cells, Humans, Oncogenes.
Abstract
Chloroquine (CQ) is an antimalarial drug and late-stage inhibitor of autophagy currently FDA-approved for use in the treatment of rheumatoid arthritis and other autoimmune diseases. Based primarily on its ability to inhibit autophagy, CQ and its derivative, hydroxychloroquine, are currently being investigated as primary or adjuvant therapy in multiple clinical trials for cancer treatment. Oncogenic RAS has previously been shown to regulate autophagic flux, and cancers with high incidence of RAS mutations, such as pancreatic cancer, have been described in the literature as being particularly susceptible to CQ treatment, leading to the hypothesis that oncogenic RAS makes cancer cells dependent on autophagy. This autophagy "addiction" suggests that the mutation status of RAS in tumors could identify patients who would be more likely to benefit from CQ therapy. Here we show that RAS mutation status itself is unlikely to be beneficial in such a patient selection because oncogenic RAS does not always promote autophagy addiction. Moreover, oncogenic RAS can have opposite effects on both autophagic flux and CQ sensitivity in different cells. Finally, for any given cell type, the positive or negative effect of oncogenic RAS on autophagy does not necessarily predict whether RAS will promote or inhibit CQ-mediated toxicity. Thus, although our results confirm that different tumor cell lines display marked differences in how they respond to autophagy inhibition, these differences can occur irrespective of RAS mutation status and, in different contexts, can either promote or reduce chloroquine sensitivity of tumor cells.
DOI: 10.4161/auto.32135
PubMed: 25136801
Affiliations:
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pubmed:25136801Le document en format XML
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<series><title level="j">Autophagy</title>
<idno type="eISSN">1554-8635</idno>
<imprint><date when="2014" type="published">2014</date>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Autophagy (drug effects)</term>
<term>Cell Line, Tumor</term>
<term>Cell Proliferation (drug effects)</term>
<term>Chloroquine (pharmacology)</term>
<term>HEK293 Cells</term>
<term>Humans</term>
<term>Lung Neoplasms (pathology)</term>
<term>Oncogenes</term>
<term>Phagosomes (drug effects)</term>
<term>Phagosomes (metabolism)</term>
<term>Tumor Suppressor Protein p53 (metabolism)</term>
<term>ras Proteins (metabolism)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Autophagie ()</term>
<term>Cellules HEK293</term>
<term>Chloroquine (pharmacologie)</term>
<term>Humains</term>
<term>Lignée cellulaire tumorale</term>
<term>Oncogènes</term>
<term>Phagosomes ()</term>
<term>Phagosomes (métabolisme)</term>
<term>Prolifération cellulaire ()</term>
<term>Protéine p53 suppresseur de tumeur (métabolisme)</term>
<term>Protéines G ras (métabolisme)</term>
<term>Tumeurs du poumon (anatomopathologie)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Tumor Suppressor Protein p53</term>
<term>ras Proteins</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Chloroquine</term>
</keywords>
<keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Tumeurs du poumon</term>
</keywords>
<keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Autophagy</term>
<term>Cell Proliferation</term>
<term>Phagosomes</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Phagosomes</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Phagosomes</term>
<term>Protéine p53 suppresseur de tumeur</term>
<term>Protéines G ras</term>
</keywords>
<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Lung Neoplasms</term>
</keywords>
<keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Chloroquine</term>
</keywords>
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<term>HEK293 Cells</term>
<term>Humans</term>
<term>Oncogenes</term>
</keywords>
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<term>Cellules HEK293</term>
<term>Humains</term>
<term>Lignée cellulaire tumorale</term>
<term>Oncogènes</term>
<term>Phagosomes</term>
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<front><div type="abstract" xml:lang="en">Chloroquine (CQ) is an antimalarial drug and late-stage inhibitor of autophagy currently FDA-approved for use in the treatment of rheumatoid arthritis and other autoimmune diseases. Based primarily on its ability to inhibit autophagy, CQ and its derivative, hydroxychloroquine, are currently being investigated as primary or adjuvant therapy in multiple clinical trials for cancer treatment. Oncogenic RAS has previously been shown to regulate autophagic flux, and cancers with high incidence of RAS mutations, such as pancreatic cancer, have been described in the literature as being particularly susceptible to CQ treatment, leading to the hypothesis that oncogenic RAS makes cancer cells dependent on autophagy. This autophagy "addiction" suggests that the mutation status of RAS in tumors could identify patients who would be more likely to benefit from CQ therapy. Here we show that RAS mutation status itself is unlikely to be beneficial in such a patient selection because oncogenic RAS does not always promote autophagy addiction. Moreover, oncogenic RAS can have opposite effects on both autophagic flux and CQ sensitivity in different cells. Finally, for any given cell type, the positive or negative effect of oncogenic RAS on autophagy does not necessarily predict whether RAS will promote or inhibit CQ-mediated toxicity. Thus, although our results confirm that different tumor cell lines display marked differences in how they respond to autophagy inhibition, these differences can occur irrespective of RAS mutation status and, in different contexts, can either promote or reduce chloroquine sensitivity of tumor cells. </div>
</front>
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<name sortKey="Morgan, Shellie" sort="Morgan, Shellie" uniqKey="Morgan S" first="Shellie" last="Morgan">Shellie Morgan</name>
<name sortKey="Staskiewicz, Leah" sort="Staskiewicz, Leah" uniqKey="Staskiewicz L" first="Leah" last="Staskiewicz">Leah Staskiewicz</name>
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<name sortKey="Thorburn, Jacqueline" sort="Thorburn, Jacqueline" uniqKey="Thorburn J" first="Jacqueline" last="Thorburn">Jacqueline Thorburn</name>
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